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Question For E. Coli Long-Term Evolution Experiment


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#81 aelyn

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Posted 19 June 2012 - 12:39 AM

Ok aelyn, that was a pretty long post, maybe you haven't got the time to reply. In summary I feel that I have dealt with evidence you have put forward concerning extra coding genes that are beneficial to an organism, especially the "proof" of human/ape common ancestry.

I feel I may have missed one or two of your links while focusing on other links, feel free to re-post any links I've missed so we can discuss if they contain any evidence of the evolutionary process.

Well I have been quite busy lately but the main reason I haven't answered your post is that I'm not sure how to. You accused me of semantics when I was just trying to clarify what you meant so I didn't argue against things you don't believe, which I find extremely dispiriting. We also seem to be disagreeing about the very basics of how genetics work (...maybe) and I need to think about how to address that without just repeating my previous post. I'm also worried that here you talk about proof of human/ape ancestry when I'm certainly not interested in any "proof". And responding to your posts usually takes a lot of research so that takes energy :) I do want to reply to your post, it might just take a few more days.

#82 NewPath

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Posted 19 June 2012 - 02:47 AM

Well I have been quite busy lately but the main reason I haven't answered your post is that I'm not sure how to. You accused me of semantics when I was just trying to clarify what you meant so I didn't argue against things you don't believe, which I find extremely dispiriting. We also seem to be disagreeing about the very basics of how genetics work (...maybe) and I need to think about how to address that without just repeating my previous post. I'm also worried that here you talk about proof of human/ape ancestry when I'm certainly not interested in any "proof". And responding to your posts usually takes a lot of research so that takes energy Posted Image I do want to reply to your post, it might just take a few more days.


No problem aelyn. Please don't misunderstand my mention of semantics as an accusation, its was just an expression of my frustration with communication and word meanings, its so easy to misunderstand eachother's meaning. And please cherry-pick my post, hopefully we cut down on a few discussion topics because it does take energy.

#83 aelyn

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Posted 19 June 2012 - 10:37 AM

Thank you for your patience NewPath ^^
And thanks for explaining your conception of “species”. I would appreciate it if you looked in detail into the chimpanzee, gorilla, gibbon and macaque genomes and got back to me with your observations. In aggregate the chimpanzee genome is more like the human genome than it is like the gorilla or gibbon genome, and especially the macaque genome. They're also different in their chromosomal organisation; macaques have 40 chromosomes while the great apes have 48, and the equivalent DNA segments are distributed all over the place IIRC. But I don't know what any of that means for “chromosomal patterns”, hence the need for your analysis. (note also that dogs are incredibly similar genetically speaking, which makes sense in that they diverged very recently. No comparison with the aggregate difference we find between gorillas and macaques).

I have a question about this sentence though : “If you have unique active beneficial genes in each organism with no signs that they both has these same coding regions, this would show differing species, not a sub-species”. How about beneficial genes that have a non-coding equivalent in another organism's genome ? That is, sequences of DNA that are almost identical in both organisms but with small differences that make them a coding gene in one and a non-coding sequence in the other, would those indicate differing species ?

As for the paper, you're asking “who really cares about what the authors say” after making such a big deal of their use of the word “indel” ? The thing is, if using the word required the assumptions you say then the paper would never have been written. Using the word the way you say wouldn't be a contradiction in their arguments, it would indicate they don't believe their own conclusion in the first place ! And the fact is, you can't know directionality just from looking at the sequences, you need additional arguments to show that directionality. So if they were indeed using “indel” as a term that implies directionality they would need to defend and justify their use of that term. In fact they'd need to write a whole paper explaining why they think the mutations happened in the direction their use of “indel” implies. Kind of like the paper they did write, except completely opposite... Not even that actually because they also refer to “enablers” in the human genes.
It looks like they used the term indel a lot like in its “original use and meaning” according to Wikipedia :

In systematics, researchers could find differences between sequences, such as from two different species. But it was impossible to infer if one species lost the sequence or the other gained it. For example, species A has a run of 4 G nucleotides at a locus and species B has 5 G's at the same locus. If the mode of selection is unknown, we can't tell if species A lost one G (a “deletion” event) or species B gained one G (an “insertion” event). When we cannot infer the phylogenetic direction of the sequence change, the sequence change event is referred to as an “indel”.

Actually it looks like at some point they refer to the same mutation as being an “enabler” in humans and a “disabler” in gorillas and gibbons. Overall the whole paper uses the words “enabling” and “disabling” interchangeably, with the former being used when they consider the coding version of the sequences and the latter when they consider the non-coding version.

I'm not asking you to agree with the paper's conclusions – of course you disagree with the paper's conclusions :) But here we aren't disagreeing on the paper's conclusions, we're disagreeing on what it says in the first place. And I see no reason why we should disagree about that.

And I don't agree we're talking about a single mutation. The paper clearly refers to several mutations. There is a part where they refer to the “chimp and macaque sequences sharing one disabler” for three genes, maybe that's what you mean ? It seems there were specific mutations they were looking for but they aren't the only ones there – the whole section following the reference to those “one disabler”s also talks about “shared sequence differences” in the gene spanning the disabler. Definitely a plural.

Thank you also for giving cites for the Duffy gene; from what you were saying it wasn't clear at all whether all the different inactive alleles were inactive because of the same mutation but reading the relevant papers it does seem that is the case, and it also seems that mutation occurred independently in Africa and in Papua New Guinea. I don't know about two independent origins in Africa; the Wikipedia page says so but the paper they link to explicitly says they cannot say why there are two haplotypes, and independent origin is just one of several hypotheses they propose. It's from 2000 there might be a more recent paper somewhere but I coudn't find one.

Their studies are full of terms like “these are added genes from the common ancestor”. In each case the unbiased reader has to ignore all those phrases and look only at the evidence presented

Except that the study we're talking about does not, in fact, say “these are added genes from the common ancestor”. Even worse, it uses words that might appear to imply such directionality (“disablers”, “enablers”, “indels”) completely inconsistently, which suggests they are not using those words to imply directionality at all. I absolutely agree the unbiased reader has to ignore all those phrases and look only at the evidence presented. Why then am I the one saying we should focus on their argument while you talk about two words that they used ?

If I have said impossible, let me re-phrase that to: currently not observed, and not logically likely because duplication of function would more likely be neutral or cause damage through a logical projection of novel genes being coding.

OK, I'll try to keep that clarification in mind ^^. So since your argument is about likelihoods I need to know what you base that “not logically likely” thing. We're not talking about the odds of a given mutation or duplication being beneficial here; we're talking about the odds of one sequence of duplication and mutations being beneficial overall, given all of the duplications and mutations that happen in all organisms over many generations. For the probability such an event to be under 50%, the probability of a single mutation being beneficial would have to be incredibly low. How low do you feel it is ?

As for being a neutralist, do you appreciate how precise a position that is ? Neutral drift has the beauty of being random, and random things are very very amenable to statistical analysis. Neutral drift makes precise predictions for what the genome should look like. It's not completely foolproof (random mutations aren't always quite random, there are apparently mutation hotspots and things like that) but it works well enough that we can tell sections of the genome that underwent neutral drift from sections that didn't, and even date the point of divergence between related groups. The paper that looked at the Duffy antigen in Africans and Italians talked a lot about that actually.
Do you see the neutral theory of molecular evolution as a theory with predictive power, and are you aware of the kinds of predictions it makes, why, and how those have been tested ?

Active protein-protein interaction means the gene is functioning, two identical duplicated genes functioning at the same time cause excess proteins and therefore excess activity in one particular area of an organism that should have a balance, and therefore if you duplicate active genes you decrease the fitness of the organism.

Yeah, I was pretty baffled as to how to respond to this without just repeating what I'd said earlier, but then reading the paper on the Papua New Guineans I was reminded of one little thing : people are diploid. Every time there are two alleles that code for a subtly different protein, or one of them doesn't code for a protein at all, the population will be polymorphic on how many proteins are expressed just because people will be homozygous for different alleles and many will be heterozygous. And most of those differences in the amount of proteins will be neutral, or slightly beneficial or harmful depending on the environment. I mean, you know this, it's the kind of thing that variations in eye and hair color are made of. But even if we look at a single chromosome, humans vary on the number of copies they have of many genes (www.gene-quantification.de/cnv-faq.pdf). The relevant googleable term is “copy number variation”. A relevant quote from the paper : “It was startling to discover that 12% of the human genome was copy number variable in the 270 DNA samples tested. About 2900 genes, or 10% of those known, are encompassed by these CNVs. Some CNVs found in the general population can be millions of bases in size, affecting numerous genes, yet they have no observable consequence”.

So no, there is nothing OBVIOUS about damage being caused by variable amounts of protein expression or duplicate genes. Sometimes it is, sometimes it isn't.

Beneficial mutations occur, but they involve destroyed genes or adapted genes, not new genes.

Yes, that is the kind of beneficial mutation I was thinking of when I said I thought we'd agreed beneficial mutations can happen. But thank you for confirming.

Okay, I'd like to propose two scenarios :
(1) Organism contains protein-coding gene A.
(2) Organism undergoes a gene duplication for gene A, resulting in gene A and gene A'
(2a) Gene A' does not get expressed, which means it's basically a noncoding stretch of DNA : the duplication has no effect on the phenotype
(2b) Both gene A and gene A' are expressed and the effect on the phenotype is selectively neutral
(3a) Mutations accumulate on the noncoding stretch of DNA corresponding to gene A' including some that modify it in a beneficial ways and that make it be expressed again, yielding new beneficial gene B.
(3b) Mutations accumulate on gene A', including beneficial ones that adapt it for a novel purpose, changing it to gene B.
(4ab) Organism contains two different protein-coding genes A and B that together have more functions than gene A had on its own.

I'd like to know which of these steps you think are too unlikely. It seems to me you might object to either (2a) → (3a) (a stretch of noncoding DNA becoming a new gene), or (2) → (2b) (active duplicate genes being selectively neutral); is that it or do you have other problems with those scenarios ?

My wording is clear, “extra beneficial non-viral coding genes”. Evolution has no evidence of this, let's not get confused by my wording when its so clear

Whether I'm too stupid to understand your so-clear wording or you're being confusing or we're just both on slightly different wavelengths, if I ask for clarification it's because I need clarification. In this case I'll go with the “different wavelengths” interpretation, I had misunderstood something from the beginning (I'd been talking about duplicates as if they didn't count as extra genes, beneficial or no, and I thought you did too but looking back at previous posts I see things were more ambiguous than I thought) and I must not have expressed the reason I was confused well enough because your responses didn't really address my problem. But I think I've gotten it straight now :)

#84 NewPath

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Posted 20 June 2012 - 11:50 AM

Thank you for your patience NewPath ^^
And thanks for explaining your conception of “species”. I would appreciate it if you looked in detail into the chimpanzee, gorilla, gibbon and macaque genomes and got back to me with your observations. In aggregate the chimpanzee genome is more like the human genome than it is like the gorilla or gibbon genome, and especially the macaque genome. They're also different in their chromosomal organisation; macaques have 40 chromosomes while the great apes have 48, and the equivalent DNA segments are distributed all over the place IIRC. But I don't know what any of that means for “chromosomal patterns”, hence the need for your analysis. (note also that dogs are incredibly similar genetically speaking, which makes sense in that they diverged very recently. No comparison with the aggregate difference we find between gorillas and macaques).


When I say chromosomal pattern I mean chromosomal organisation. I will take your word for it that they are all so dissimilar, so then they would all be different species, unrelated except by similarities in chromosomal organisation and so similarities in their look function and behaviour.

I have a question about this sentence though : “If you have unique active beneficial genes in each organism with no signs that they both has these same coding regions, this would show differing species, not a sub-species”. How about beneficial genes that have a non-coding equivalent in another organism's genome ? That is, sequences of DNA that are almost identical in both organisms but with small differences that make them a coding gene in one and a non-coding sequence in the other, would those indicate differing species ?


Well you should be catching onto the big picture now. I've already acknowledged duplications, and de-coding of genes, a sub-species can easily be created through a mutation and isolation. If the only difference between an ape and a human was a non-coding region then I would say same species. Chromosomal polymorphism can result in sub-species as well. These changes can be selected, but rarely. I would guess that normally they come about through some sort of isolation and bottleneck affect whereby the new population is too isolated from the previous population for the mutation to be de-selected as would normally occur in a larger population. Due to the chromosomal organisation being different in the new population, there can be difficulties breeding between the two populations, and different coloring etc in the new sub-species.

As for the paper, you're asking “who really cares about what the authors say” after making such a big deal of their use of the word “indel” ? The thing is, if using the word required the assumptions you say then the paper would never have been written. Using the word the way you say wouldn't be a contradiction in their arguments, it would indicate they don't believe their own conclusion in the first place ! And the fact is, you can't know directionality just from looking at the sequences, you need additional arguments to show that directionality. So if they were indeed using “indel” as a term that implies directionality they would need to defend and justify their use of that term. In fact they'd need to write a whole paper explaining why they think the mutations happened in the direction their use of “indel” implies. Kind of like the paper they did write, except completely opposite... Not even that actually because they also refer to “enablers” in the human genes.
It looks like they used the term indel a lot like in its “original use and meaning” according to Wikipedia :
Actually it looks like at some point they refer to the same mutation as being an “enabler” in humans and a “disabler” in gorillas and gibbons. Overall the whole paper uses the words “enabling” and “disabling” interchangeably, with the former being used when they consider the coding version of the sequences and the latter when they consider the non-coding version.


Well if they want to make a good point they should say what they mean. It also wouldn't be the first time a self -defeating argument has been put forward, so even if their argument is self -defeating this does not give us the right to assume they meant differently to their own wording. The only argument against it being coding first is the fact that it developed in different organisms. I dealt with that argument with my "Duffy gene" argument, that recent mutations can occur at the same place in the human genome amongst independent but recently dispersed populations. There is no reason to preclude that possibility in apes. That set of genes across a few species of apes could have experienced de-coding pressures that no longer exist due to the elimination of the threat. So whether we look at the word "indels" or at their other arguments for concluding the non-coding region came first, their arguments are not conclusive. You are too focussed on my "indel" argument, I'm looking at ANY reason those scientists could have to declare the non-coding region came first. Their own wording has some ambiguity, that's not my main point.

OK, I'll try to keep that clarification in mind ^^. So since your argument is about likelihoods I need to know what you base that “not logically likely” thing. We're not talking about the odds of a given mutation or duplication being beneficial here; we're talking about the odds of one sequence of duplication and mutations being beneficial overall, given all of the duplications and mutations that happen in all organisms over many generations. For the probability such an event to be under 50%, the probability of a single mutation being beneficial would have to be incredibly low. How low do you feel it is ?


Your point is too subjective for me, evolution is a theory, based on possibilities and projections of events that are unobserved. Its impossible to quantify when no rates of novel unique new beneficial genes are ever recorded. Even if one day we observe ONE instance, you cannot project rates based on a single instance. Unquantifiable and most likely never to occur. I cannot give you percentages of the chances of a non-existent process suddenly existing. I call evolution an interesting hypothesis", nothing more, its merely an idea. Something like fairies, they could exist, how do we know? (ps I'm stirring here :-)

Please do not find holes in my illustration, just try to understand me better by my illustration:
Imagine a 100% automated car factory. It produces cars, but over time it gets a bit faulty through lack of maintenance. Imagine the gaps on the sparkplugs get smaller because that robot is exerting slightly too much pressure. Efficiency of the vehicles decreases. But imagine a change of atmosphere where the gap actually helps the engine run better. The faulty old assembly line has produced an improvement. It can happen. But it is absolutely impossible for all the random possible improvements to produce a steadily improving vehicle. The vehicles will always get worse given time or stay the same unless a designer redesigns the process. Yes slight rare occasional improvements can accidently happen, but these are unnatural freaks caused by organisms having to adapt to an environment they were not exposed to before.


As for being a neutralist, do you appreciate how precise a position that is ? Neutral drift has the beauty of being random, and random things are very very amenable to statistical analysis. Neutral drift makes precise predictions for what the genome should look like. It's not completely foolproof (random mutations aren't always quite random, there are apparently mutation hotspots and things like that) but it works well enough that we can tell sections of the genome that underwent neutral drift from sections that didn't, and even date the point of divergence between related groups. The paper that looked at the Duffy antigen in Africans and Italians talked a lot about that actually.
Do you see the neutral theory of molecular evolution as a theory with predictive power, and are you aware of the kinds of predictions it makes, why, and how those have been tested ?


Actually I'm not aware of how precise it is, I was just interested that there was a theory out there that covered most of what I'm saying, but believe that is an unnecessary divergence to our main focus, and I wouldn't want my own views to be restricted at this stage to any one theory.


So no, there is nothing OBVIOUS about damage being caused by variable amounts of protein expression or duplicate genes. Sometimes it is, sometimes it isn't.

You seem to be missing the point here, by using the word "OR"

I am looking for positive GROWTH in the genome, because the genome needs to grow if a bacteria becomes human. Not changes to alleles, which may affect protein expression as the different alleles are designed to do.

It is obvious that more protein expression within the duplicate gene would be damaging. Changing an allele is not duplicating a function, ADDING an active allele would be duplicating a function, causing damage. Adding a duplicate coding gene even more so.





Okay, I'd like to propose two scenarios :
(1) Organism contains protein-coding gene A.
(2) Organism undergoes a gene duplication for gene A, resulting in gene A and gene A'
(2a) Gene A' does not get expressed, which means it's basically a noncoding stretch of DNA : the duplication has no effect on the phenotype
(2b) Both gene A and gene A' are expressed and the effect on the phenotype is selectively neutral
(3a) Mutations accumulate on the noncoding stretch of DNA corresponding to gene A' including some that modify it in a beneficial ways and that make it be expressed again, yielding new beneficial gene B.
(3b) Mutations accumulate on gene A', including beneficial ones that adapt it for a novel purpose, changing it to gene B.
(4ab) Organism contains two different protein-coding genes A and B that together have more functions than gene A had on its own.

I'd like to know which of these steps you think are too unlikely. It seems to me you might object to either (2a) → (3a) (a stretch of noncoding DNA becoming a new gene), or (2) → (2b) (active duplicate genes being selectively neutral); is that it or do you have other problems with those scenarios ?


Will answer this tomorrow if I get the chance.


Whether I'm too stupid to understand your so-clear wording or you're being confusing or we're just both on slightly different wavelengths, if I ask for clarification it's because I need clarification. In this case I'll go with the “different wavelengths” interpretation, I had misunderstood something from the beginning (I'd been talking about duplicates as if they didn't count as extra genes, beneficial or no, and I thought you did too but looking back at previous posts I see things were more ambiguous than I thought) and I must not have expressed the reason I was confused well enough because your responses didn't really address my problem. But I think I've gotten it straight now Posted Image

I think my wording is confusing.

#85 NewPath

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Posted 20 June 2012 - 01:23 PM

Okay, I'd like to propose two scenarios :
(1) Organism contains protein-coding gene A.
(2) Organism undergoes a gene duplication for gene A, resulting in gene A and gene A'
(2a) Gene A' does not get expressed, which means it's basically a noncoding stretch of DNA : the duplication has no effect on the phenotype
(2b) Both gene A and gene A' are expressed and the effect on the phenotype is selectively neutral
(3a) Mutations accumulate on the noncoding stretch of DNA corresponding to gene A' including some that modify it in a beneficial ways and that make it be expressed again, yielding new beneficial gene B.
(3b) Mutations accumulate on gene A', including beneficial ones that adapt it for a novel purpose, changing it to gene B.
(4ab) Organism contains two different protein-coding genes A and B that together have more functions than gene A had on its own.

I'd like to know which of these steps you think are too unlikely. It seems to me you might object to either (2a) → (3a) (a stretch of noncoding DNA becoming a new gene), or (2) → (2b) (active duplicate genes being selectively neutral); is that it or do you have other problems with those scenarios ?

Good point. I see you are trying to find some logical way your theory of evolution can actually work in practice. Interesting that intelligent educated evolutionists do not all know the hypothetical process. I feel both cases are unlikely because they involve duplicating functions of sequences of nucleotides (instead of entire genes). The same protein over-expression applies.

I believe a logical projection of point B) is that a major natural mutation to a nucleotide sequence that activates it would be destructive without the help of an intelligent designer, because how can random major changes have a spontaneously good effect? And a minor adjustment would retain the protein duplication effects that cause damage.

Evolution is like projecting a duck building a city. Its possible that a duck by mistake knocks a stone on top of another stone and it looks like a human placed them there. But no matter how many ducks you project onto how many planets, they are never going to spontaneously create a city. New DNA sequences with novel functions do not spontaneously arise from just exponential multiplication over 600 million years. You first have to observe the beneficial protein-coding insertion rate, and then exponentially project it to make evolution viable over even a 600 million year period. With an observed rate of zero, its all just fantasy.

#86 aelyn

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Posted 20 June 2012 - 03:47 PM

Well you should be catching onto the big picture now. I've already acknowledged duplications, and de-coding of genes, a sub-species can easily be created through a mutation and isolation. If the only difference between an ape and a human was a non-coding region then I would say same species. Chromosomal polymorphism can result in sub-species as well. These changes can be selected, but rarely. I would guess that normally they come about through some sort of isolation and bottleneck affect whereby the new population is too isolated from the previous population for the mutation to be de-selected as would normally occur in a larger population. Due to the chromosomal organisation being different in the new population, there can be difficulties breeding between the two populations, and different coloring etc in the new sub-species.

Thank you for the precision. I went back to the list of differences you mentioned between chimpanzees and humans, including additional active genes in chimpanzees on several chromosomes. I tried to look that up but my google-fu wasn't up to the task... Would you mind giving me a specifics for one or two of those ?

Well if they want to make a good point they should say what they mean.

As far as I can tell they do. I really think your interpretation of the word "indel" does not reflect their usage, and given the Wikipedia page I do think their usage of the word is well-understood in their field.

It also wouldn't be the first time a self -defeating argument has been put forward, so even if their argument is self -defeating this does not give us the right to assume they meant differently to their own wording. The only argument against it being coding first is the fact that it developed in different organisms. I dealt with that argument with my "Duffy gene" argument, that recent mutations can occur at the same place in the human genome amongst independent but recently dispersed populations. There is no reason to preclude that possibility in apes.

Except that the probability of several mutations happening independently in four groups is orders of magnitude smaller than the probability of a single mutation happening in two groups (or even three, frankly).

That set of genes across a few species of apes could have experience de-coding pressures that no longer exist due to the elimination of the threat.

It's true selection pressures change the likelihoods to some extent (the odds of the mutation happening are the same, but it's more likely to stick around), but there are many different ways of disabling a gene. Selection pressures for disabling a gene on their own won't necessarily yield the same mutations disabling the gene.

So whether we look at the word "indels" or at their other arguments for concluding the non-coding region came first, their arguments are not conclusive. You are too focussed on my "indel" argument, I'm looking at ANY reason those scientists could have to declare the non-coding region came first. Their own wording has some ambiguity, that's not my main point.

I was responding to your "indel" argument because you were making it; I agree you also addressed their actual argument and I responded to that too, but I did feel you were putting a lot of emphasis on the "indel" thing, hence responding to it as I did. I'm glad we're focusing on more relevant things now. I don't expect to convince you of the validity of the argument because it does rely on accepting common descent to some extent, but my original point (If I recall correctly lol) was that the authors did have an argument, they weren't just arbitrarily going "oh those must be new human genes". I'm fine with discussing the validity of the argument though, insofar as I can explain why it would be convincing to geneticists (if not to you).

Your point is too subjective for me, evolution is a theory, based on possibilities and projections of events that are unobserved. Its impossible to quantify when no rates of novel unique new beneficial genes are ever recorded. Even if one day we observe ONE instance, you cannot project rates based on a single instance. Unquantifiable and most likely never to occur. I cannot give you percentages of the chances of a non-existent process suddenly existing. I call evolution an interesting hypothesis", nothing more, its merely an idea. Something like fairies, they could exist, how do we know? (ps I'm stirring here :-)

But if we think beneficial genes come from duplication and subsequent modifications to one or both of the duplicate genes (which is not the only possibility as I'm realizing more and more from reading up on this, but it is considered one mechanism), then that could theoretically be quantified as both duplications and modifications leading to beneficial changed genes have been recorded. In general if you can't directly observe something, or often enough for statistical significance, but you have a mechanism you can find out about its likelihood by looking at the likelihood of the mechanism.

Now I think the actual quantifications that have been done were based on analyzing existing genomes and inferring past rates of duplications and beneficial changes but I'm not certain, I haven't looked it up yet.

Please do not find holes in my illustration, just try to understand me better by my illustration:
Imagine a 100% automated car factory. It produces cars, but over time it gets a bit faulty through lack of maintenance. Imagine the gaps on the sparkplugs get smaller because that robot is exerting slightly too much pressure. Efficiency of the vehicles decreases. But imagine a change of atmosphere where the gap actually helps the engine run better. The faulty old assembly line has produced an improvement. It can happen. But it is absolutely impossible for all the random possible improvements to produce a steadily improving vehicle. The vehicles will always get worse given time or stay the same unless a designer redesigns the process. Yes slight rare occasional improvements can accidently happen, but these are unnatural freaks caused by organisms having to adapt to an environment they were not exposed to before.

If I understand correctly you are illustrating how it is impossible for mutations that happen to be beneficial in some environment to add up to each other ? I'm not seeing anything like duplicate genes in there, or new beneficial genes, so it seems to me that's what you're saying.
I'm sorry but if that's what you mean by your illustration I can't help but find a hole in it Posted Image Namely, your illustration does not strike me as an accurate analogy for evolution in that you don't have heredity. In your illustration the single change that made the sparkplugs smaller and thus the cars run better in the changed atmosphere can't add up with other changes that might make the cars run better in the atmosphere, because all the changes in the manufacturing process happen at random and don't get propagated. If for example assembly lines were regularly getting destroyed and a machine rebuilt them depending on how efficient the cars they'd produced had been, so that it built many copies of assembly lines that had produced cars that ran better and few or no copies of the assembly lines that produced cars that ran badly, then after the atmosphere changed the machine would build more of the assembly line that produced smaller smartplugs - until most of the assembly lines did that. And as the assembly lines (that now mostly produced small sparkplugs) continued to deteriorate, every time a deterioration happened to lead to better-running cars in the new atmosphere it would also get multiplied by the machine, until most of the machines (which already had smaller sparkplugs) ALSO that other useful deterioration - so traits that led the cars to run better under the changed atmosphere could add up.
This is actually a great description of how genetic algorithms work. They're routinely used for optimization work for problems where you have no clue what an optimal solution might look like (the reason for this is that they're really not that good compared to heuristic-based techniques; the only thing worse than them is a random search basically. But when you have no heuristic i.e. no advance idea whatsoever of what the solution might look like, they're almost the only thing you could use aside from a random search, so suddenly they're pretty interesting indeed). A system with a number of solutions that get incrementally modified and whose distribution in the next generation depends on how well they match certain criteria can lead to the modifications adding up and the solutions matching the criteria better and better with subsequent generations. I say "can" because genetic algorithms can be fiddly to set up, but with the right set-up those modifications do add up and do lead to overall improvement over time. ("improvement" being defined in GAs as "better matching the criteria we're looking for", and in biological evolution would correspond to "better at reproducing in the environment they're in")

But as I said earlier that's about whether beneficial mutations can add up or not, I'm uncertain as to the link with new beneficial genes or duplicates.

Actually I'm not aware of how precise it is, I was just interested that there was a theory out there that covered most of what I'm saying, but believe that is an unnecessary divergence to our main focus, and I wouldn't want my own views to be restricted at this stage to any one theory.

That makes sense. I do wonder though what your opinion is on mutation rates. Would you agree with the scientific consensus on mutation rates (that they're mostly constant, and that what variation there is (and there is quite an amount IIRC) is where geneticists have determined it is, using their geneticist methods), or do you think that factors that aren't accounted for in mainstream genetics (like the Fall, or the flood, or random divine intervention) affected those rates in ways you can't quantify ?
Even if we assume God created separate kinds with different genomes, if we can know anything about their mutation rates since then then neutrality theory and other theories of molecular evolution would have all kinds of testable implications.

You seem to be missing the point here, by using the word "OR"

I am looking for positive GROWTH in the genome, because the genome needs to grow if a bacteria becomes human. Not changes to alleles, which may affect protein expression as the different alleles are designed to do.

It is obvious that more protein expression within the duplicate gene would be damaging. Changing an allele is not duplicating a function, ADDING an active allele would be duplicating a function, causing damage. Adding a duplicate coding gene even more so.

I'm not sure what's wrong with my "or", since you seemed to be saying that active duplicate genes were harmful because they led to different protein expressions and variations in protein expression were harmful.

Alleles are genes too, and if you have one on each chromosome that means you have two of that gene. To take an example, if we have a coding allele and a non-coding allele for a protein that yield neutral or almost-negligible differences in people and there's a gene-dosage effect then some people will have 0% of that protein being expressed (homozygous for the inactive allele, i.e. no active gene), some will have 100% (heterozygous, i.e. one active gene) and some will have 200% (homozygous for the active allele, i.e. 2 active genes).
A mutation on the active allele that led to a tandem duplication of that gene so that now you'd have two active genes where there had been one wouldn't be damaging to anyone who was heterozygous for example. Their phenotype for that gene would be just like that of a person homozygous for the normal allele.

But that example aside, are you saying that all of the polymorphisms that exist in humans today on protein expression levels are "built in" so that any variation within that polymorphism has little consequence, while any variation outside that polymorphism is necessarily damaging ?

I think my wording is confusing.

Nah, it seems to me you were answering my questions fine, you just weren't addressing my wrong assumption so I kept being confused despite your reasonable answers. To my credit I did mention the assumption I had doubts about from the beginning but given it's something I was apparently focusing on more than you were I'm not surprised you didn't address it. I mean, the question of whether we should call duplicate genes "extra genes" or not is legitimately ambiguous, I don't think you were particularly confusing on it. I just made a wrong assumption. But thanks for being charitable and all Posted Image

Interesting that intelligent educated evolutionists do not all know the hypothetical process.

That I know of, anyone who talks about "duplication and subsequent mutation" is thinking about one of these scenarios or a variant of them.

I feel both cases are unlikely because they involve duplicating functions of sequences of nucleotides (instead of entire genes). The same protein over-expression applies.

I'm not sure what you mean by that. Duplications can happen to any length of nucleotide sequences, including entire genes, several entire genes, or parts of a gene. In this scenario I'm just considering the duplication of a single gene (...you could include some non-coding sequences around it but I don't think it's that relevant). What do you mean by drawing a distinction between "sequences of nucleotides" and "entire genes" in this context ?

I believe a logical projection of point Posted Image is that a major natural mutation to a nucleotide sequence that activates it would be destructive without the help of an intelligent designer, because how can random major changes have a spontaneously good effect? And a minor adjustment would retain the protein duplication effects that cause damage.

From what I've been able to tell the difference between a non-expressed and expressed nucleotide sequence can be a small one - a frameshift, a stop codon replaced by an amino-acid-coding codon, something about ORFs. Am I correct in thinking that, as earlier, you are arguing that a change in protein expression necessarily yields large and damaging changes in the organism ?

#87 NewPath

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Posted 21 June 2012 - 01:13 AM

Thank you for the precision. I went back to the list of differences you mentioned between chimpanzees and humans, including additional active genes in chimpanzees on several chromosomes. I tried to look that up but my google-fu wasn't up to the task... Would you mind giving me a specifics for one or two of those ?


Actually I don't know where to find detailed analysis of genome sequencing. I just looked at a comparative image and the two genomes matched quite well and in detail, but having significant differences. From my creationist perspective I'm assuming design differences.


Except that the probability of several mutations happening independently in four groups is orders of magnitude smaller than the probability of a single mutation happening in two groups (or even three, frankly).

It depends on the pressures. If malaria attacked everyone in Africa and was deadly , we would only have a disabled Duffy gene population. To cause such a common disabling among large apes, my assumption would be a deadly and universal large ape disease related to that area of the genome, possibly causing extinctions among nearly every large ape species, except those populations that already had a few members with that disabling mutation. This would cause a bottleneck and then subsequent proliferation of the new mutation. This is not like the theory of evolution, I have put forward proof of simultaneous disablers, and projected possibilities based on actual observations.

I was responding to your "indel" argument because you were making it; I agree you also addressed their actual argument and I responded to that too, but I did feel you were putting a lot of emphasis on the "indel" thing, hence responding to it as I did. I'm glad we're focusing on more relevant things now. I don't expect to convince you of the validity of the argument because it does rely on accepting common descent to some extent, but my original point (If I recall correctly lol) was that the authors did have an argument, they weren't just arbitrarily going "oh those must be new human genes". I'm fine with discussing the validity of the argument though, insofar as I can explain why it would be convincing to geneticists (if not to you).

Well if their argument relies on accepting common descent, and you are using that argument to prove common descent, then that's definite circular reasoning, which ironically is what most arguments for evolution are based on. Your point that the authors did have an argument is already dealt with when I showed that the Duffy gene can express itself in independent populations. If there is no more points left for you to make, kindly admit that this human/ape non-coding argument is not conclusive and therefore should be dropped from our discussion, because we are starting to repeat ourselves.

But if we think beneficial genes come from duplication and subsequent modifications to one or both of the duplicate genes (which is not the only possibility as I'm realizing more and more from reading up on this, but it is considered one mechanism), then that could theoretically be quantified as both duplications and modifications leading to beneficial changed genes have been recorded. In general if you can't directly observe something, or often enough for statistical significance, but you have a mechanism you can find out about its likelihood by looking at the likelihood of the mechanism.


Well looking at the mechanism, it looks unlikely to me, likely to you, is that what evolution is based on?? A projection that appears likely to biased observers? That is in the realm of fantasy and not science, to me the processes involve likely protein over expression, hence damage. Or the creation of a functional unique sequence out of nothing which is in the realm of the supernatural.

If I understand correctly you are illustrating how it is impossible for mutations that happen to be beneficial in some environment to add up to each other ? I'm not seeing anything like duplicate genes in there, or new beneficial genes, so it seems to me that's what you're saying.

Well the unlikelihood of the appearance of an extra beneficial coding gene through mutation ever occurring is slim, never being observed in any organism. Therefore the possibility of two such occurring to the same organism is exponentially unlikely and we have no timeframes to base this on. 3 even more unlikely. The whole process is therefore unlikely even using evolutionary timeframes.

I'm sorry but if that's what you mean by your illustration I can't help but find a hole in it Posted Image


I'm not even responding to this, there are always holes in imperfect comparisons, so it doesn't take a rocket scientist to point out the holes. It does take maturity to learn the other's position better by gaining further understanding from illustrations.

That makes sense. I do wonder though what your opinion is on mutation rates. Would you agree with the scientific consensus on mutation rates (that they're mostly constant, and that what variation there is (and there is quite an amount IIRC) is where geneticists have determined it is, using their geneticist methods), or do you think that factors that aren't accounted for in mainstream genetics (like the Fall, or the flood, or random divine intervention) affected those rates in ways you can't quantify ?
Even if we assume God created separate kinds with different genomes, if we can know anything about their mutation rates since then then neutrality theory and other theories of molecular evolution would have all kinds of testable implications.


My personal assumption is an escalation of damaging mutations since the flood, because the life-spans of humans deteriated from 900 years old to 70 years old. I don't know enough, but I think this is related to atmospheric oxygen and pressure levels, whereby cells were better cleansed and rejuvenated under old atmospheres where the oxygen content can be better retained in the bloodstream due to air pressures greater than 1 ATM. So there was damage at the fall and then further damage at the flood. I believe science would benefit by looking into these possibilities and re-assessing their studies based on biblical assumptions, it can be surprising what they may find when putting on a new thinking cap. You may just find that all humans have a common ancestor, mutation rates are high, there are more extinctions observed than new species, the genome battles to favorably increase the number of coding genes. No wait! Devolution is already observed, yet evolution is assumed to be true anyway.

Alleles are genes too, and if you have one on each chromosome that means you have two of that gene. To take an example, if we have a coding allele and a non-coding allele for a protein that yield neutral or almost-negligible differences in people and there's a gene-dosage effect then some people will have 0% of that protein being expressed (homozygous for the inactive allele, i.e. no active gene), some will have 100% (heterozygous, i.e. one active gene) and some will have 200% (homozygous for the active allele, i.e. 2 active genes).

Ok I'm still learning the new terminology, the whole subject is new to me. I misunderstood an allele to be an expression of variants in nucleotides, not entire genes. Its making more sense now.

But that example aside, are you saying that all of the polymorphisms that exist in humans today on protein expression levels are "built in" so that any variation within that polymorphism has little consequence, while any variation outside that polymorphism is necessarily damaging ?

Not really. I'm saying it would seem logical to me that any duplicate sequences that are active are damaging, no matter where you find that duplicate sequence. It could be within a gene, in two genes, in two chromosomes. Some sequences are more important than other sequences, some chromosomes more important than others, but generally the larger the duplicate coding sequence, the more damage. We are designed with a set number of coding nucleotides, duplicate these and you overexpress proteins, decrease the number and you lose some functionality. Dramatically change the workings of a coding sequence through mutation without a designer, and you have a distortion. These are the observable processes in the reality of molecular biology. Sometimes its helpful to lose functionality because disease can attack a function. But generally its all bleak, devolving and not evolving.

I'm not sure what you mean by that. Duplications can happen to any length of nucleotide sequences, including entire genes, several entire genes, or parts of a gene. In this scenario I'm just considering the duplication of a single gene (...you could include some non-coding sequences around it but I don't think it's that relevant). What do you mean by drawing a distinction between "sequences of nucleotides" and "entire genes" in this context ?

Some sequences can be duplicated without entire genes being duplicated. You would have the same problem but on a smaller scale.


From what I've been able to tell the difference between a non-expressed and expressed nucleotide sequence can be a small one - a frameshift, a stop codon replaced by an amino-acid-coding codon, something about ORFs. Am I correct in thinking that, as earlier, you are arguing that a change in protein expression necessarily yields large and damaging changes in the organism ?


No , I'm generally quite a logical person Posted Image Generally a small change in protein expression causes small damage, a large change, large damage.

#88 gilbo12345

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Posted 21 June 2012 - 07:27 AM

Simply put the DNA % analysis argument for evolution is based on the assumption that evolution is true. There is no definitive mechanism that can be empirically demonstrated therefore the claimed mechanism of evolution is merely assumed. As has been mentioned using this "evidence" to "prove" evolution is circular reasoning.

The complexity argument of DNA can be enhanced further by a few things

1- Each coding area of DNA comes with its own signal system, in which specific environmental conditions outside or within the cell will activate the production of that gene's product. ie- a ribosome is damaged and gets recycled there is a need to replace it, membrane damage has occured and new transport proteins are required in the newly created portion of membrane...etc etc.

The fact that generally each gene has its own signal system brings complications for the evolutionists.

i) how did the signal system "evolve" at the same time as the function of the gene
ii) how did the cell / signal system "know" what environmental factors would be required for the proper use of this specific gene product

Furthermore, when it is claimed that DNA within organisms can alter and change, this also has its own problem since in order to get new biological systems to evolve, new functions would be needed... However with new functions, new signal systems would also be required. Unless changes to both are proposed to occur simultaneously, (which are not statistically possible), then there would be a period in which the new function would have a less than optimal signal system. An analogy would be if you ordered a steering wheel online, and the seller kept of sending you a car tyre instead, both are round but they have different functions. Logically this would lead to a decrease in fitness, (thus defying the natural selection concept).



2. There is no naturalistic cause for the information within DNA. Naturalists must admit that information within DNA is an anathema to the very concept of evolution since evolutionary dogma states that evolution is an unguided, undirected process therefore considering that there is no unguided / undirected naturalistic process that can create information in the same form as DNA, (ie- code / blueprints for building / maintenance )... Then there is no naturalistic reason for information within DNA, which would therefore run as an observed and confirmed contradiction to naturalistic evolution.
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#89 aelyn

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Posted 23 June 2012 - 12:01 PM

I'm sorry this post is so long, I went on like five different essays that I don't really want to cut :(

Actually I don't know where to find detailed analysis of genome sequencing. I just looked at a comparative image and the two genomes matched quite well and in detail, but having significant differences. From my creationist perspective I'm assuming design differences.

I don't see how much you can get from a comparative image; those I saw on google were quite small, and basically consisted of chromosomes with bands on them. I'm not clear on what those bands represent but they seem to be regions of the chromosome (centromeres, telomeres, AT-rich zones vs GC-rich zones), not individual genes. That seems to make them useless for comparing genes, let alone making sure genes in one species don't correspond to noncoding sequences in the other.
Do you have a link to the specific image you're thinking of, maybe it's clearer than those I've found ?

It depends on the pressures. If malaria attacked everyone in Africa and was deadly , we would only have a disabled Duffy gene population. To cause such a common disabling among large apes, my assumption would be a deadly and universal large ape disease related to that area of the genome, possibly causing extinctions among nearly every large ape species, except those populations that already had a few members with that disabling mutation. This would cause a bottleneck and then subsequent proliferation of the new mutation. This is not like the theory of evolution, I have put forward proof of simultaneous disablers, and projected possibilities based on actual observations.

Selection makes it more likely that disablers will stick around but it doesn't affect the probability of a specific set of disabling mutations happening independently of each other much. As I've said, the probability for a single mutation happening twice is low but not that low; the probability for several mutations happening four times is orders of magnitude lower. Selecting for disablers can help a bit, but unless you're selecting for those specific disabling mutations (which you can't be if the gene is disabled, because mutations to a disabled gene are neutral, thus any mutation that would disable the gene is selected for to the same extent, you can't select for a specific one) it won't help enough.

Well if their argument relies on accepting common descent, and you are using that argument to prove common descent, then that's definite circular reasoning, which ironically is what most arguments for evolution are based on.

I am not using that argument to prove common descent at all ! I brought up that study when you said that current observations showed genomes were deteriorating. I assumed that you were getting those “current observations” from geneticists and said that geneticists disagree.
The point is, when geneticists say genes are being damaged, or deleted, or inserted by viruses, they are using the exact same arguments, reasoning and assumptions as when they say genes are being created. If you don't like the reasoning of the people who wrote that paper on new human genes you should explain to me why you like the reasoning of, for example, the people who say the human genome contains ERVs.

Well looking at the mechanism, it looks unlikely to me, likely to you, is that what evolution is based on?? A projection that appears likely to biased observers? That is in the realm of fantasy and not science, to me the processes involve likely protein over expression, hence damage. Or the creation of a functional unique sequence out of nothing which is in the realm of the supernatural.

I'm not talking about just “looking” at the mechanism. The point is we can try and find out how likely or unlikely it is.
It's hard to quantify the probability of a mutation being beneficial vs deleterious or neutral, especially since whether a mutation is beneficial or not depends on the environment, but many beneficial mutations (not beneficial new genes, I'm talking single mutations here. New genes (excluding unmodified duplicates of course) don't arise in a single generation) have been observed in all kinds of organisms from bacteria to humans. Neutral and deleterious mutations have been observed to be A LOT more common of course, but the fact we've been able to observe beneficial mutations in the first place in the short time that we've been looking indicates their odds may be low, but not vanishingly low.
Similarly, non-damaging duplications are known to happen. I haven't found much in the way of actual probabilities (I would have thought that has been calculated; I'll continue looking), but considering things like 10% of the human genome having a different number of copies between individuals it can't be very low either.
So I'm not seeing how the odds of a beneficial mutation happening on a part of the genome that's the result of a previous duplication are so low it wouldn't happen in one of thousands of individuals in thousands of generations.

Well the unlikelihood of the appearance of an extra beneficial coding gene through mutation ever occurring is slim, never being observed in any organism. Therefore the possibility of two such occurring to the same organism is exponentially unlikely and we have no timeframes to base this on. 3 even more unlikely. The whole process is therefore unlikely even using evolutionary timeframes.

Just to make sure : we're not talking about the odds of two beneficial mutations happening in the same organism, as in “the same individual”. It is a very important thing to understand about evolution, that it doesn't all happen in a single generation. In particular, nobody is proposing that new genes arise in a single generation.
The question is the probability of two beneficial mutations (I'll talk about mutations here because they can happen in a single generation, but the argument is substantially the same for new genes) happening in the same lineage, i.e. an organism has a beneficial mutation, then its great-great-grandorganism (which inherited its ancestor's mutation) gets another beneficial mutation, which means it now has two that it will pass on to its own descendants.
The thing is the probability of two beneficial mutations happening successively in a lineage isn't the product of the probability of each one happening on its own, because the two events aren't independent. A beneficial mutation is much more likely to occur in a lineage that already contains beneficial mutations, i.e. in an organism that has inherited beneficial mutations from its ancestor. Why is that ? Because an ancestor that had a beneficial mutation had more descendants than its contemporaries, and that mutation spreads throughout the population over the generations, which means most organisms at the time the second mutation happens already have the first one. That's the importance of natural selection, as I explained earlier when I was using it as an example of how an additional process can change the probabilities of something happening from negligible to perfectly likely.
I don't know your math background, do you understand what I am saying here ?

I'm not even responding to this, there are always holes in imperfect comparisons, so it doesn't take a rocket scientist to point out the holes. It does take maturity to learn the other's position better by gaining further understanding from illustrations.

Analogies are made in order to help understand a certain situation, by bringing up another situation that is easier to understand but, and this is important, is like the original situation in all relevant ways.
Those make it a very important tool for thinking, not only because they clarify things but the very exercise of looking for an analogy means we need to figure out what the relevant aspects of the situations we're thinking of are and why we're drawing the conclusion we do. A good analogy is one where all the relevant aspects are represented, so conclusions taken from the analogy will apply to the original situation. A bad analogy is one that misses a relevant aspect of the situation, or has additional aspects that affect the analogy in a way the situation isn't; both of those things mean the conclusions one derive from the analogy don't necessarily apply to the situation.
Figuring out whether an analogy is good or bad, and why, is actually one of the best ways of understanding the situation at hand.
In this case it seems to me you were making an analogy for how you think evolution works, thus showing why you derived the conclusions you did about evolution. I did consider your illustration carefully and thought about why you made it (hence my questions about it). That's why I pointed out to you the very relevant aspect of evolution that was not included in your analogy, and how including it affected the conclusions one could make.
If I was misinterpreting your illustration I apologize.

My personal assumption is an escalation of damaging mutations since the flood, because the life-spans of humans deteriorated from 900 years old to 70 years old. I don't know enough, but I think this is related to atmospheric oxygen and pressure levels, whereby cells were better cleansed and rejuvenated under old atmospheres where the oxygen content can be better retained in the bloodstream due to air pressures greater than 1 ATM. So there was damage at the fall and then further damage at the flood. I believe science would benefit by looking into these possibilities and re-assessing their studies based on biblical assumptions, it can be surprising what they may find when putting on a new thinking cap. You may just find that all humans have a common ancestor, mutation rates are high, there are more extinctions observed than new species, the genome battles to favorably increase the number of coding genes.

We can calculate mutation rates right now; apparently in humans they're around 2.5 per 100,000,000 base pairs per generation. Would you say those rates are the result of a steady increase since the flood (i.e. the rates we calculate now are higher than the mutation rates were in the past), or that there was a spike at some point after the flood and mutation rates today are lower ?
Looking at the human genome today, with the current assumptions on the rate of mutation we get humans having had a genetic bottleneck of something like 15,000 people 70,000 years ago, and different genes having “coalescence points” (which I assume to be a “common ancestor”, but for genes) ranging from 2 million years ago to 60,000 years ago. (none of this requires assuming common descent, other than common descent of all humans which we agree on)
If we assume instead that today's mutation rates are at an all-time high, then those estimates need to be revised upward, i.e. if genes were mutating more slowly in the past, then they took more time to become as they are than we currently think.
If we assume that mutations rates were higher in the past then those would be over-estimates, but to get those times down to 10,000 or 6000 or 4000 years (when do you say the flood happened ?) then the mutation rates have to be assumed to have been very high indeed, and we know that too-high mutation rates cause cancer and birth defects.
Also, oxygen does pretty much the opposite of “rejuvenating”. It's a very aggressive oxidant, as the name suggests. This makes it perfect for powering our metabolism but it also makes it harmful to our actual tissues. The only way it can be said to “rejuvenate” is that it makes the body work harder to repair tissues, which may be why high-pressure oxygen therapy is good for injuries, but it's no good in the long term (in fact apparently people doing hyperbaric oxygen therapy need “air breaks” once in awhile to avoid oxygen toxicity). (source for all the numbers is Wikipedia)

Not really. I'm saying it would seem logical to me that any duplicate sequences that are active are damaging, no matter where you find that duplicate sequence. It could be within a gene, in two genes, in two chromosomes. Some sequences are more important than other sequences, some chromosomes more important than others, but generally the larger the duplicate coding sequence, the more damage. We are designed with a set number of coding nucleotides, duplicate these and you overexpress proteins, decrease the number and you lose some functionality. Dramatically change the workings of a coding sequence through mutation without a designer, and you have a distortion. These are the observable processes in the reality of molecular biology. Sometimes its helpful to lose functionality because disease can attack a function. But generally its all bleak, devolving and not evolving.

Yet we find all kinds of duplicate sequences in humans that aren't damaging (I'm talking about copy number variations, not alleles here).

We agree that large changes will usually have damaging effects, but evolution isn't about large changes happening in a single generation, it's about small changes building up over many generations.

#90 NewPath

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Posted 23 June 2012 - 04:44 PM

I don't see how much you can get from a comparative image; those I saw on google were quite small, and basically consisted of chromosomes with bands on them. I'm not clear on what those bands represent but they seem to be regions of the chromosome (centromeres, telomeres, AT-rich zones vs GC-rich zones), not individual genes. That seems to make them useless for comparing genes, let alone making sure genes in one species don't correspond to noncoding sequences in the other.
Do you have a link to the specific image you're thinking of, maybe it's clearer than those I've found ?

I'm haven't got that link on this particular computer but I agree with you that the image did not give enough information. Nevertheless the human does have coding genes not found in chimps.


Selection makes it more likely that disablers will stick around but it doesn't affect the probability of a specific set of disabling mutations happening independently of each other much. As I've said, the probability for a single mutation happening twice is low but not that low; the probability for several mutations happening four times is orders of magnitude lower. Selecting for disablers can help a bit, but unless you're selecting for those specific disabling mutations (which you can't be if the gene is disabled, because mutations to a disabled gene are neutral, thus any mutation that would disable the gene is selected for to the same extent, you can't select for a specific one) it won't help enough.

You obviously did not read my explanation that well, I gave a perfectly probable explanation for independent mutations. There are great apes that have become extinct, its perfectly feasible that many great apes died off from a disease and only those with a disabled region survived. Thus an environmental factor could have selected only those apes not susceptible , through a disabling mutation. This would explain the entire situation, including the recent extinction of many great apes.

The point is, when geneticists say genes are being damaged, or deleted, or inserted by viruses, they are using the exact same arguments, reasoning and assumptions as when they say genes are being created. If you don't like the reasoning of the people who wrote that paper on new human genes you should explain to me why you like the reasoning of, for example, the people who say the human genome contains ERVs.

Your point here is illogical, each study has its own evidence and methodology when reaching their conclusions. The evidence should be looked at to see if the conclusion is logical. I am still waiting for any conclusive evidence for evolution, none of the links you have posted have actually showed any evidence. This is really what I'm interested in this discussion, I have had other evolutionists admit that this is a weakness in evolutionary theory, the lack of evidence for additional novel coding genes that benefit the fitness of the organism.

I'm not talking about just “looking” at the mechanism. The point is we can try and find out how likely or unlikely it is.
It's hard to quantify the probability of a mutation being beneficial vs deleterious or neutral, especially since whether a mutation is beneficial or not depends on the environment, but many beneficial mutations (not beneficial new genes, I'm talking single mutations here. New genes (excluding unmodified duplicates of course) don't arise in a single generation) have been observed in all kinds of organisms from bacteria to humans. Neutral and deleterious mutations have been observed to be A LOT more common of course, but the fact we've been able to observe beneficial mutations in the first place in the short time that we've been looking indicates their odds may be low, but not vanishingly low.


This all seems irrelevant to me. An escalation of deleterious mutations that assist survival could be pointing to an escalation of disease on the planet, or an escalation of vulnerability to disease. I understand that evolution does not require that every organism always becomes more complex over time, but evolution does try to explain modern complex life-forms. and this is what my argument is about. I do not see a likely process, nor an observation of this process. Without these its just an interesting theory that is popular because its a modern trend to see supernatural intervention as illogical. Its ironic that the only reason that supernatural intervention became less popular is Darwinism in the first place, before that most populations saw it as perfectly logical. So Darwinism drew science away from God, and now this lack of belief in God is keeping science away from interpreting the facts correctly, because God now seems illogical. Religion never used to seem illogical. Its also ironic that science has this "religious" belief that although we do not know where matter came from, or life, or intricate coding genes, we would rather believe in inexplicable processes than God. The evidence of the fossil record and molecular biology is pointing towards insertions of fully formed DNA based organisms onto this planet.

Similarly, non-damaging duplications are known to happen. I haven't found much in the way of actual probabilities (I would have thought that has been calculated; I'll continue looking), but considering things like 10% of the human genome having a different number of copies between individuals it can't be very low either.
So I'm not seeing how the odds of a beneficial mutation happening on a part of the genome that's the result of a previous duplication are so low it wouldn't happen in one of thousands of individuals in thousands of generations.

You may as well worship the "earth-mother" of nature, spontaneously creating completely new functions in a gene in such a manner that the duplicated protein-coding sequence does not duplicate protein-coding. Unless the entire duplicated sequence is totally unique, the extra novel coding gene will show damaging protein over-expression. How do you create a totally unique useful sequence from scratch that will NOT duplicate protein coding? You would need nature to be creative and intelligent, you would have to believe in the supernatural guiding force of "mother nature".

Just to make sure : we're not talking about the odds of two beneficial mutations happening in the same organism, as in “the same individual”. It is a very important thing to understand about evolution, that it doesn't all happen in a single generation. In particular, nobody is proposing that new genes arise in a single generation.
The question is the probability of two beneficial mutations (I'll talk about mutations here because they can happen in a single generation, but the argument is substantially the same for new genes) happening in the same lineage, i.e. an organism has a beneficial mutation, then its great-great-grandorganism (which inherited its ancestor's mutation) gets another beneficial mutation, which means it now has two that it will pass on to its own descendants.

The thing is the probability of two beneficial mutations happening successively in a lineage isn't the product of the probability of each one happening on its own, because the two events aren't independent. A beneficial mutation is much more likely to occur in a lineage that already contains beneficial mutations, i.e. in an organism that has inherited beneficial mutations from its ancestor. Why is that ? Because an ancestor that had a beneficial mutation had more descendants than its contemporaries, and that mutation spreads throughout the population over the generations, which means most organisms at the time the second mutation happens already have the first one. That's the importance of natural selection, as I explained earlier when I was using it as an example of how an additional process can change the probabilities of something happening from negligible to perfectly likely.
I don't know your math background, do you understand what I am saying here ?

You wish to project possibilities of duplicate genes over-expressing proteins in already well-balanced organisms in a beneficial manner when this has never been observed. The math of the whole situation is nonsensical. Possibilities exist, Its possible that a rabbit takes one second to knock a pebble onto another pebble accidentally. You can perfectly project the math to one rabbit accidentally building one wall of a house made from pebbles in only 45 days using that rate of one a second. That's just the illogical application of maths.

The wall of evolution is built on shaky foundations. You have no process and no timing yet you have built a fantasy projection of possibilities.


We can calculate mutation rates right now; apparently in humans they're around 2.5 per 100,000,000 base pairs per generation. Would you say those rates are the result of a steady increase since the flood (i.e. the rates we calculate now are higher than the mutation rates were in the past), or that there was a spike at some point after the flood and mutation rates today are lower ?
Looking at the human genome today, with the current assumptions on the rate of mutation we get humans having had a genetic bottleneck of something like 15,000 people 70,000 years ago, and different genes having “coalescence points” (which I assume to be a “common ancestor”, but for genes) ranging from 2 million years ago to 60,000 years ago. (none of this requires assuming common descent, other than common descent of all humans which we agree on)
If we assume instead that today's mutation rates are at an all-time high, then those estimates need to be revised upward, i.e. if genes were mutating more slowly in the past, then they took more time to become as they are than we currently think.
If we assume that mutations rates were higher in the past then those would be over-estimates, but to get those times down to 10,000 or 6000 or 4000 years (when do you say the flood happened ?) then the mutation rates have to be assumed to have been very high indeed, and we know that too-high mutation rates cause cancer and birth defects.
Also, oxygen does pretty much the opposite of “rejuvenating”. It's a very aggressive oxidant, as the name suggests. This makes it perfect for powering our metabolism but it also makes it harmful to our actual tissues. The only way it can be said to “rejuvenate” is that it makes the body work harder to repair tissues, which may be why high-pressure oxygen therapy is good for injuries, but it's no good in the long term (in fact apparently people doing hyperbaric oxygen therapy need “air breaks” once in awhile to avoid oxygen toxicity). (source for all the numbers is Wikipedia)

All your talk concerning the rates of damaging or neutral mutations is irrelevant to our discussion. I am not trying to prove every aspect of my own thoughts on the matter, my participation in this thread is to highlight the lack of proof for evolution, not to prove or disprove alternatives.
Regarding oxygen I would assume about 30% oxygen and 1.5 bar is about right considering ancient oxygen content. They are often using 100% oxygen in a 2 bar environment in modern medicine which is over-dosing. Anyway this is all beside the point.


Yet we find all kinds of duplicate sequences in humans that aren't damaging (I'm talking about copy number variations, not alleles here).

We agree that large changes will usually have damaging effects, but evolution isn't about large changes happening in a single generation, it's about small changes building up over many generations.


Even small positive changes are neither observed, nor theoretically likely. Its just an idea. Maybe it can work,but it does not seem scientifically possible because of definite logical constraints. To explain all life from a hypothesis of projecting a series of unlikely and unobserved events is a fantasy and unscientific process. Science should be evaluating other processes, the propensity not to believe in God will probably lead to the theory of "alien insertions" of life-forms on this planet, at least that would be more empirically accurate than the evolving of life.

#91 aelyn

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Posted 23 June 2012 - 08:37 PM

I'm haven't got that link on this particular computer but I agree with you that the image did not give enough information. Nevertheless the human does have coding genes not found in chimps.

Which ones ? As I said in my very first post here, I couldn't find any when I looked. I did find some in that paper we've been talking about later, but those correspond to noncoding sequences in other apes and monkeys.

You obviously did not read my explanation that well, I gave a perfectly probable explanation for independent mutations. There are great apes that have become extinct, its perfectly feasible that many great apes died off from a disease and only those with a disabled region survived. Thus an environmental factor could have selected only those apes not susceptible , through a disabling mutation. This would explain the entire situation, including the recent extinction of many great apes.

We've got four species that we're assuming do not have a common ancestor. Say they all had this coding gene in four separate ancestral populations. It got randomly disabled in some individuals of each. Then a disease came and wiped out everyone that had the coding version of the gene, so after a time each one of those species only had individuals with a disabled gene.
For those four genes to have been disabled by the exact same mutation each time you need the same mutation to have happened four times independently.
Let's say we go with that. Other mutations accumulate on that now-noncoding sequence, which means those mutations are neutral (so no selection pressure at work, be it caused by disease or anything else). For the accumulated mutations on each of those genes to be identical or almost identical they would also all need to have occurred independently in the four lineages.
And here we're talking independent, i.e. the probability of all those mutations happening is the product of the probability of each one happening on its own. It's astronomically low.
And no, a single mutation having happened two or three times independently as with the Duffy gene isn't a counter-example. Each time you add a mutation or an independent source you decrease the odds by some order of magnitude.

Your point here is illogical, each study has its own evidence and methodology when reaching their conclusions.

Okay, what evidence and methodology did this study use ? Or this one ?
Any study that purports to deduce the history of a genome (including gene losses, inactivations or ERV insertions) by comparing it with the genomes of other species (i.e. every study of this kind) relies on the assumption that there is such a history, i.e. that the species in question have a common ancestor. If each was created independently with their own independent genomes whose similarities are only coincidental then nothing historical can be deduced by comparing those genomes. Including histories of gene loss, inactivation or insertions of ERVs.

This all seems irrelevant to me. An escalation of deleterious mutations that assist survival could be pointing to an escalation of disease on the planet, or an escalation of vulnerability to disease.

You seem to be using words in an idiosyncratic way again. A deleterious mutation that assists survival isn't deleterious; the technical word to describe it is "beneficial".
You're probably talking about mutations that inactivate or delete bits of genome, but diseases are by no means the only reason such mutations can be beneficial.

You may as well worship the "earth-mother" of nature, spontaneously creating completely new functions in a gene in such a manner that the duplicated protein-coding sequence does not duplicate protein-coding. Unless the entire duplicated sequence is totally unique, the extra novel coding gene will show damaging protein over-expression.

Protein over-expression is not always damaging. You seem to assume it MUST be the case because it seems obvious to you, but I have explained why it wasn't true several times and have given several examples of different expression levels in proteins or duplicate genes not being damaging. Here are some more examples.
If you are going to repeat that claim again I will have to ask your for some evidence for it beyond "it seems obvious to me".

You wish to project possibilities of duplicate genes over-expressing proteins in already well-balanced organisms in a beneficial manner when this has never been observed. The math of the whole situation is nonsensical. Possibilities exist, Its possible that a rabbit takes one second to knock a pebble onto another pebble accidentally. You can perfectly project the math to one rabbit accidentally building one wall of a house made from pebbles in only 45 days using that rate of one a second. That's just the illogical application of maths.

Again, your analogy doesn't resemble how evolution works in critical aspects. Please apply your maths to a situation that actually has the processes at work in evolution, such as mutation, recombination, heredity, and selection.
I don't see the point of pitting assertion against assertion and would rather start on something we both understand, so please tell me : do you know what a genetic algorithm is, and how they work ?

All your talk concerning the rates of damaging or neutral mutations is irrelevant to our discussion. I am not trying to prove every aspect of my own thoughts on the matter, my participation in this thread is to highlight the lack of proof for evolution, not to prove or disprove alternatives.

And I am trying to understand your point of view and to figure out its consequences. In this case I'm trying to figure out which aspects of molecular biology you accept and which you don't; you've said early on that you thought the discoveries of molecular biology were a problem for evolution but there are also aspects of that field you disagree with, so I'd like to better understand what the dividing line is.

Regarding oxygen I would assume about 30% oxygen and 1.5 bar is about right considering ancient oxygen content. They are often using 100% oxygen in a 2 bar environment in modern medicine which is over-dosing. Anyway this is all beside the point.

30% oxygen wouldn't be rejuvenating either; for that matter 21% isn't rejuvenating. It's just the percentage our bodies are tuned to, and can compensate for (except for insofar as oxidation damage contributes to aging...). If you think it's besides the point it's fine, but I figure this is relevant to one of your personal hypotheses so it's useful to you if not to our discussion :P .

Even small positive changes are neither observed, nor theoretically likely.

You have no theoretical basis for determining their likelihood, or at least you have given none beyond "they haven't been observed" (as if the sixty years we've spent observing were enough to catch phenomena that happen on much larger timescales) (and "duplications and protein over-expression are always damaging", to be fair, except that doesn't match observations and you haven't given any evidence for it either). And "small positive changes" have been observed aplenty, from bacteria to humans. For the bacterial examples you have the usual, nylonase, citrase, etc (interestingly I found this article that actually tried to calculate rates of beneficial mutations in E.coli - coming up with 4 per billion cells per generation. Considering the number of E.coli cells and how fast they reproduce that's quite high). Human examples include the apolipoprotein mutation or the mutation in the gene for LRP5 that leads to higher bone mass. And if you want actual duplicates having small positive effects, there's always the variation in salivary amylase genes.

Science should be evaluating other processes, the propensity not to believe in God will probably lead to the theory of "alien insertions" of life-forms on this planet, at least that would be more empirically accurate than the evolving of life.

Are you referring to panspermia ? That's not a theory, there is no theory for the origin of life, just hypotheses. Now there could have been a theory of "not-common descent", with different groups of organisms descending from independent ancestors. It wouldn't in any way have contradicted the theory of evolution by natural selection; in fact Gould proposed this exact thing regarding the Ediacaran fauna.
Do you know why biologists think there was common descent of all known life on Earth instead ?

#92 NewPath

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Posted 25 June 2012 - 05:42 AM

Which ones ? As I said in my very first post here, I couldn't find any when I looked. I did find some in that paper we've been talking about later, but those correspond to noncoding sequences in other apes and monkeys.


Check out this diagram, the differences in the human and chimp chromosome Y:
http://johnhawks.net...hughes-2010.png
Posted Image

We've got four species that we're assuming do not have a common ancestor. Say they all had this coding gene in four separate ancestral populations. It got randomly disabled in some individuals of each. Then a disease came and wiped out everyone that had the coding version of the gene, so after a time each one of those species only had individuals with a disabled gene.
For those four genes to have been disabled by the exact same mutation each time you need the same mutation to have happened four times independently.
Let's say we go with that. Other mutations accumulate on that now-noncoding sequence, which means those mutations are neutral (so no selection pressure at work, be it caused by disease or anything else). For the accumulated mutations on each of those genes to be identical or almost identical they would also all need to have occurred independently in the four lineages.
And here we're talking independent, i.e. the probability of all those mutations happening is the product of the probability of each one happening on its own. It's astronomically low.
And no, a single mutation having happened two or three times independently as with the Duffy gene isn't a counter-example. Each time you add a mutation or an independent source you decrease the odds by some order of magnitude.


I'm not aware of other identical mutations across those four species that occur within that disabled sequence , could you post that information again. Remember that a creationist believes that similar animals were created similar. In addition we are still learning about the functionality of non-coding sequences, this is a new area of research. Some non-coding sequences have been shown to have no selection pressure and others have indicated selection pressure. Indicating that there are functions that were previously assumed to be mere "junk DNA" duplicates. My point is that some similarities across similar animals could be functional and NOT mutations, God-designed beneficial parts of the genome that are similar across similar species.

Other than your point about ADDITIONAL mutations within that disabled region of those 4 apes, the 3 independent Duffy mutations and the 4 independent ape mutations are not that different, disabling mutations do occur regularly and will proliferate given selection pressure. The disabled gene seems to relate specifically to "chronic lymphocytic leukemi" which is found in large apes. I assume they didn't sequence DNA from a sickly ape, they should try genome sequencing on a gibbon with chronic lymphocytic leukemi and see if they actually do find that region disabled across all members of the population. There's a good chance that isolated populations of Gibbon still retain coding in that region, just like a human retains that region, because in isolated populations they have not had the greater numbers of mutations and subsequent selection opportunities that are available in more widespread populations.



Okay, what evidence and methodology did this study use ? Or this one ?
Any study that purports to deduce the history of a genome (including gene losses, inactivations or ERV insertions) by comparing it with the genomes of other species (i.e. every study of this kind) relies on the assumption that there is such a history, i.e. that the species in question have a common ancestor. If each was created independently with their own independent genomes whose similarities are only coincidental then nothing historical can be deduced by comparing those genomes. Including histories of gene loss, inactivation or insertions of ERVs.

The problem with that methodology is that evolution automatically assumes everything HAS to be added, nothing is original. You then have to have a theory behind when and how each part of the genome was added, and then evolutionists look for similar organisms to try and determine the timing of the differences between them. If the underlying assumption is incorrect, some of the conclusions will be incorrect,


You seem to be using words in an idiosyncratic way again. A deleterious mutation that assists survival isn't deleterious; the technical word to describe it is "beneficial".
You're probably talking about mutations that inactivate or delete bits of genome, but diseases are by no means the only reason such mutations can be beneficial.

I did use the word incorrectly, I thought "deleterious" related to deletions. Yes I've always admitted that deletions can be beneficial, which does not assist the theory of "common descent", but indicates reducing complexity over time as more genes are deleted or inactive and these become selected into the population. Disease related deletions/disabling that are naturally selected are surprisingly common but I have no problem with deletions serving other purposes as well. This can indicate common ancestry among sub-species but is some sort of devolving and not evolving (reduced complexity over time).


Protein over-expression is not always damaging. You seem to assume it MUST be the case because it seems obvious to you, but I have explained why it wasn't true several times and have given several examples of different expression levels in proteins or duplicate genes not being damaging. Here are some more examples.
If you are going to repeat that claim again I will have to ask your for some evidence for it beyond "it seems obvious to me".

The first link is concerning organisms that are already damaged due to altered protein, these organism benefit from genes that can restore damaged protein levels. This is not a net gain, but restoration of a loss of function, also emphasizing the need for stable protein coding levels.



The second link is about transgenic mice. This is not a natural process and in transgenic cases we often see an immediate benefit (juicy seedless fruit) but this does not tell much about the improved general fitness of that organism in nature compared to wild-types. ie the artificial hybrid mice could have reduced fitness in nature even though they have improved resistance to heart disease.

Neither case concerns a duplicate gene that duplicates protein coding.

Again, your analogy doesn't resemble how evolution works in critical aspects. Please apply your maths to a situation that actually has the processes at work in evolution, such as mutation, recombination, heredity, and selection.
I don't see the point of pitting assertion against assertion and would rather start on something we both understand, so please tell me : do you know what a genetic algorithm is, and how they work ?

Not in detail, i understand the concept. Its really applying logical exponential principles to genetic hypotheses.


And I am trying to understand your point of view and to figure out its consequences. In this case I'm trying to figure out which aspects of molecular biology you accept and which you don't; you've said early on that you thought the discoveries of molecular biology were a problem for evolution but there are also aspects of that field you disagree with, so I'd like to better understand what the dividing line is.

The whole field of molecular biology is new and to reach definite conclusions is too premature based on current evidence. I have no clear dividing line except to look at actual studies and see what common sense can be made of these studies if you remove evolutionary assumptions. I feel that is a pretty logical approach to the whole matter. I must frustrate creationists because in their eyes I may be re-inventing the wheel, because my learning does not come from creationist websites, but from re-interpreting scientific evidence from a creationist perspective. I hold the evidence as highly informative, the interpretations as sometimes faulty.

Genome sequencing as a whole is highlighting devolution rather than evolution, damaging insertions and improving deletions are prevalent, as is a high mutation rate. Beneficial mutations are rare and never involve coding insertions that cause overall fitness improvements of the organism. So the evidence is pointing to devolution. The natural prediction of biological devolution are more extinctions than new species over time, which is supported by the fossil record.

You have no theoretical basis for determining their likelihood, or at least you have given none beyond "they haven't been observed" (as if the sixty years we've spent observing were enough to catch phenomena that happen on much larger timescales) (and "duplications and protein over-expression are always damaging", to be fair, except that doesn't match observations and you haven't given any evidence for it either). And "small positive changes" have been observed aplenty, from bacteria to humans. For the bacterial examples you have the usual, nylonase, citrase, etc (interestingly I found this article that actually tried to calculate rates of beneficial mutations in E.coli - coming up with 4 per billion cells per generation. Considering the number of E.coli cells and how fast they reproduce that's quite high). Human examples include the apolipoprotein mutation or the mutation in the gene for LRP5 that leads to higher bone mass. And if you want actual duplicates having small positive effects, there's always the variation in salivary amylase genes.

No idea why you keep quoting examples of beneficial mutations. I believe in a process of the last surviving species on this earth (modern species) adapting to protect from disease and fill unique ecological gaps by losing complexity over time, and sometimes gaining non-coding duplications to add hardiness. I believe strongly in this natural selection and adaptation process. As an organism becomes extinct another organism has to fill that ecological gap and may lose some active genes to reduce in size, or reduce a function, or change an allele frequency to fill that gap. I do believe this can even involve limited macro-evolution, but through the observed processes of decreasing complexity over time, and changes to allele frequencies, not through increased protein-coding complexity over time. I believe this theory is observed, and your links confirm these beneficial mutations that I do believe in. Its only the theory of increased complexity from common ancestors that I disagree with, I do agree with minor observed decreased complexity and also non-coding duplications from recent common ancestors..

An interesting fact from your one link is that independent mutations often occur at the same place in the genome, a point we have discussed often in this thread:
Nonsyndromic high bone mass has been linked to 11q12–13 in another kindred.16 While we were preparing this report, Little et al. identified an LRP5 mutation in the other kindred.32 Remarkably, this mutation is identical to the LRP5V171 mutation in our kindred. To our knowledge, these families do not share a common ancestor, suggesting that the mutations have arisen independently; however, the possibility of a very remote common ancestor cannot be excluded

#93 aelyn

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Posted 25 June 2012 - 11:02 AM

Check out this diagram, the differences in the human and chimp chromosome Y:

Yes, the Y chromosome is very particular. I'd like to look more into it before responding, but in the meantime have you read the webpage associated with that picture ?

I'm not aware of other identical mutations across those four species that occur within that disabled sequence , could you post that information again.

You're right, I confused myself on that one; I think the plurals in the paper I was interpreting as several mutations per gene were referring to the mutations on the three genes. In fact when I think about it I think I was dead wrong indeed evolutionarily speaking : if the sequences had been as I was saying then the chimps, macaques, gorillas etc would be more like each other than chimps are like humans... and that would upend the classification of apes :) (well, probably not for a single gene, but it would be surprising). Given mutations to non-functional DNA are neutral, if it took several mutations to make a sequence functional the first ones would have to accumulate neutrally, i.e. slowly, i.e. not all at once after humans and chimpanzees had diverged.

Looking at the specific differences in question however they do seem like specific changes I wouldn't expect to see happening five times independently, especially the last one :
The enabling/disabling mutation for the first gene is one A nucleotide in the chimpanzee, gibbon, macaque and gorilla genomes vs none in the human (i.e. a deletion in the human genome, or the independent insertion of the same nucleotide in the same place four times). For the second gene it's one C nucleotide in humans vs a T nucleotide in chimps, gorillas, orang-utans, gibbons and macaques (i.e. one substitution in humans, or five independent substitutions to the same nucleotide in five species). And for the third one it's ten base pairs that are present in humans but not in chimps, gorillas, orang-utans, gibbons or macaques (i.e. one 10-bp insertion in humans, or the deletion of exactly the same 10 base pairs in five independent species).


But yeah I do think I was wrong on the several mutations thing, sorry about that.

Remember that a creationist believes that similar animals were created similar. In addition we are still learning about the functionality of non-coding sequences, this is a new area of research. Some non-coding sequences have been shown to have no selection pressure and others have indicated selection pressure.

Yes, hence why I've been questioning your focus on protein-coding genes. But molecular biologists have ways to differentiate between functional and nonfunctional sequences. It's true that looking at the selection pressures is a big one... but I'm surprised to see you bring that up. Do you understand how people tell a sequence that's under selection pressure from one that isn't ?
I ask because it involves comparing the genomes of different species in a way that's only meaningful if we assume those species are actually related. I think it also involves assumptions on mutation rates that are similar to what we use for molecular clocks.

Indicating that there are functions that were previously assumed to be mere "junk DNA" duplicates. My point is that some similarities across similar animals could be functional and NOT mutations, God-designed beneficial parts of the genome that are similar across similar species.

Of course. There's just no evidence for it.

Other than your point about ADDITIONAL mutations within that disabled region of those 4 apes, the 3 independent Duffy mutations and the 4 independent ape mutations are not that different, disabling mutations do occur regularly and will proliferate given selection pressure.

For one thing I still don't know that they're 3 independent Duffy mutations and not two. For another, I do think the insertion of a specific nucleotide and especially the deletion of the same 10 base pairs is different from a substitution. (the actual probabilities depend on how genes work but offhand a substitution in a specific place involves changing to one of three base pairs while an insertion is one of four, and deleting the same 10 bp sounds much less likely than deleting or subsituting the same 1)
Interesting quote about the LRP5 gene; I hadn't picked up on that when reading it. Note that they think it's "remarkable" to find the same mutation twice, and don't dare to rule out a common ancestor.

The disabled gene seems to relate specifically to "chronic lymphocytic leukemi" which is found in large apes. I assume they didn't sequence DNA from a sickly ape, they should try genome sequencing on a gibbon with chronic lymphocytic leukemi and see if they actually do find that region disabled across all members of the population.


I don't get it, are you saying when the gene's active it causes chronic lymphocytic leukemia ? I don't think the humans they were looking at were sickly either.

The problem with that methodology is that evolution automatically assumes everything HAS to be added, nothing is original. You then have to have a theory behind when and how each part of the genome was added, and then evolutionists look for similar organisms to try and determine the timing of the differences between them. If the underlying assumption is incorrect, some of the conclusions will be incorrect.

Evolution doesn't assume everything HAS to be added; in fact I'm pretty sure people who work in abiogenesis research would say there were sets of "original" genes that arose at some point along the process. But can say practically nothing about stuff that far back.

Of course when looking at the genes of, say, chimpanzees it's pretty clear most of them have been "added" since the primordial genomes; that's not an assumption, it's a consequence of common descent. And I understand you think common descent is an assumption but that is actually not true either, it's a conclusion derived from observations.
Creationists disagree with the derivation of course, but I asked in my previous post and I'd still like to know, do you understand how and why biologists came to the conclusion of common descent ?

I did use the word incorrectly, I thought "deleterious" related to deletions.

Ha ! I'd never thought of that but that's a perfectly reasonable assumption. It's a stupid word really :)

The first link is concerning organisms that are already damaged due to altered protein, these organism benefit from genes that can restore damaged protein levels. This is not a net gain, but restoration of a loss of function, also emphasizing the need for stable protein coding levels.
The second link is about transgenic mice. This is not a natural process and in transgenic cases we often see an immediate benefit (juicy seedless fruit) but this does not tell much about the improved general fitness of that organism in nature compared to wild-types. ie the artificial hybrid mice could have reduced fitness in nature even though they have improved resistance to heart disease.

Resistance to diseases is a benefit, and "transgenic" doesn't mean "magic", they're still mice with mousy metabolisms that use proteins; if over-expression was always harmful it should harm them too. You're basically saying that changes in protein expression are always harmful, and if we don't observe them to be harmful, well, they must be anyway, look harder.
That's great but as I said I would like an actual source on your claims now.

Neither case concerns a duplicate gene that duplicates protein coding.

The reason you gave for why coding duplicate genes would be harmful was because of protein over-expression. Is there some other reason ? Or is protein overexpression caused by duplicate genes somehow different from protein overexpression caused by something else ?

Not in detail, i understand the concept. Its really applying logical exponential principles to genetic hypotheses.

Okay... I'm not sure what you mean by that at all. Which genetic hypotheses are you thinking of, and what are "logical exponential principles" ?

I'll leave the rest aside, I don't think my replies bring much that we haven't gone over before and I'm interested in your answers to my questions about genetic algorithms and common descent.

#94 NewPath

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Posted 26 June 2012 - 12:51 AM

You're right, I confused myself on that one; I think the plurals in the paper I was interpreting as several mutations per gene were referring to the mutations on the three genes. In fact when I think about it I think I was dead wrong indeed evolutionarily speaking : if the sequences had been as I was saying then the chimps, macaques, gorillas etc would be more like each other than chimps are like humans... and that would upend the classification of apes Posted Image (well, probably not for a single gene, but it would be surprising). Given mutations to non-functional DNA are neutral, if it took several mutations to make a sequence functional the first ones would have to accumulate neutrally, i.e. slowly, i.e. not all at once after humans and chimpanzees had diverged.

Looking at the specific differences in question however they do seem like specific changes I wouldn't expect to see happening five times independently, especially the last one :
The enabling/disabling mutation for the first gene is one A nucleotide in the chimpanzee, gibbon, macaque and gorilla genomes vs none in the human (i.e. a deletion in the human genome, or the independent insertion of the same nucleotide in the same place four times). For the second gene it's one C nucleotide in humans vs a T nucleotide in chimps, gorillas, orang-utans, gibbons and macaques (i.e. one substitution in humans, or five independent substitutions to the same nucleotide in five species). And for the third one it's ten base pairs that are present in humans but not in chimps, gorillas, orang-utans, gibbons or macaques (i.e. one 10-bp insertion in humans, or the deletion of exactly the same 10 base pairs in five independent species).


But yeah I do think I was wrong on the several mutations thing, sorry about that.


No problem. Now the problem with your logic about the second gene and third gene being mutations, is that your logic does not deal with the possibility that the C nucleotide and the T nucleotide and the 10 base pair difference were created like that. Your logic assumes common descent and therefore assumes a mutation rather than a created difference across all 3 genes, whereas a neutral observer without the assumption of common descent would definitely see the mutation in gene 1 and not in gene 2 and 3. The only part that is definitely a mutation is the precise matching and yet non-coding region in apes which shows a pre-existing and matching sequence between the species and yet subsequent change.

I don't get it, are you saying when the gene's active it causes chronic lymphocytic leukemia ? I don't think the humans they were looking at were sickly either.

If you do not get this basic point I feel like shutting down the whole discussion. This is the basis for my whole Duffy gene argument and its shocking to me that I have wasted so many posts with you when you are not getting basic points. The Duffy gene argument shows that malaria is associated with a certain gene. Its not that the gene CAUSES malaria, its more likely that malaria proliferates in the functions of the human body that the particular gene codes for. Humans are therefore better off with that function DEAD if we live in malaria ridden areas. Mutations occur regularly, statistically with only 22000 genes and populations of millions, every now and then a certain gene is switched off in a human due to regular mutation. Most genes would undergo this. If ever a deleted gene can be favorable, this mutation can proliferate through selective pressure to protect a population against a disease.

Now apply the same logic to apes who have susceptibility to chronic lymphocytic leukemia. The very article you originally quoted did state that the particular region we are discussing that is non-coding in apes is specifically associated with chronic lymphocytic leukemia. In isolated populations Gibbons are still battling with this disease. A similar situation could be occurring whereby a disabling mutation occurred to that set of genes and assisted the apes with reduced susceptibility to chronic lymphocytic leukemia. This is what a neutral observer would be seeing, a region of the genome that is quite similar across a few species, yet subsequently disabled in some species in the very area of the genome associated with a killer disease.

In the meantime you keep bringing up the point that the Duffy gene may only be independent in 2 populations and not 3, which frankly appears nitpicky. I assumed you were a person who wants to make progress in these discussions and instead I have to re-explain my points and get distracted by side-issues. Your human/ape common descent argument is far from conclusive given ability of genes to mutate (and become selected) into non-coding regions in cases when a population is under threat from a deadly disease. The fact that even the original article you cited states that this gene is associated with a specific disease strengthens my point.

Before we go any further I would like you to acknowledge that your human/ape common descent argument is not conclusive, my points have sufficiently covered all your objections.

#95 aelyn

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Posted 26 June 2012 - 08:40 AM

No problem. Now the problem with your logic about the second gene and third gene being mutations, is that your logic does not deal with the possibility that the C nucleotide and the T nucleotide and the 10 base pair difference were created like that.

I am talking about your suggestion that those non-coding sequences corresponded to an ancestral coding gene that had been disabled independently in the species other than humans; that's the possibility my logic is dealing with. We can consider other possibilities if you wish but that will involve other arguments. And in fact I have addressed “the genes could have been created that way”; I said that I have no quarrel whatsoever with people who think that.

Your logic assumes common descent and therefore assumes a mutation rather than a created difference across all 3 genes, whereas a neutral observer without the assumption of common descent would definitely see the mutation in gene 1 and not in gene 2 and 3. The only part that is definitely a mutation is the precise matching and yet non-coding region in apes which shows a pre-existing and matching sequence between the species and yet subsequent change.

I'm not sure what you're talking about; why would a neutral observer see a mutation in gene 1 (the point indel) and not in gene 2 (the substitution) or gene 3 (the 10-bp indel) ? All of those sequences involve bits that match (the vast majority) and bits that are different.
And I'm not sure why a neutral observer assuming special creation of each of those species would think any mutation had happened at all. Couldn't each of those sequences have been created as they are ?

If you do not get this basic point I feel like shutting down the whole discussion. This is the basis for my whole Duffy gene argument and its shocking to me that I have wasted so many posts with you when you are not getting basic points. The Duffy gene argument shows that malaria is associated with a certain gene. Its not that the gene CAUSES malaria, its more likely that malaria proliferates in the functions of the human body that the particular gene codes for. Humans are therefore better off with that function DEAD if we live in malaria ridden areas. Mutations occur regularly, statistically with only 22000 genes and populations of millions, every now and then a certain gene is switched off in a human due to regular mutation. Most genes would undergo this. If ever a deleted gene can be favorable, this mutation can proliferate through selective pressure to protect a population against a disease.

Yes, I do understand genes being disabled because of selection pressure to protect against a disease. If you're so frustrated at constantly re-explaining things we already both know maybe you could try and actually understand what my objection is. Namely, selection pressure for disabling a gene is not the same thing as selection pressure for a specific mutation to disable that gene, like a T to C substitution in the GATA box of the promoter for the Duffy gene B. Selection acts on the phenotype, and the phenotype “no Duffy antigen” can potentially correspond to many different mutations, so seeing the same mutation, not just the same gene being disabled but the same mutation doing so happening many times independently is surprising. Less surprising than if there had been no selection at all, but still surprising.
Now if you can show me that the T to C substitution of the GATA box of the promoter for the Duffy gene B is in fact the only possible way of disabling that gene (so that “disabling the gene” and “that mutation disabling the gene” are the same thing), or that there is a mutation hotspot that makes that particular substitution very likely, then it will be another story.
Two of the sequences the article looks at actually illustrate that, as the authors focus on one disabler/enabler for each sequence but for two of them there are several elements of the chimp or macaque sequences that keep them from being coding. What's a start codon in sequence 2 and 3 for the humans and chimps is not so in the macaque because of a substitution, and both the macaque and chimp have frameshift-causing indels in sequence 2. Any one of those things on its own would render the sequence noncoding.

Now apply the same logic to apes who have susceptibility to chronic lymphocytic leukemia. The very article you originally quoted did state that the particular region we are discussing that is non-coding in apes is specifically associated with chronic lymphocytic leukemia. In isolated populations Gibbons are still battling with this disease.

That's fascinating, could you show me where to find out more ? I couldn't find anything on that.

A similar situation could be occurring whereby a disabling mutation occurred to that set of genes and assisted the apes with reduced susceptibility to chronic lymphocytic leukemia. This is what a neutral observer would be seeing, a region of the genome that is quite similar across a few species, yet subsequently disabled in some species in the very area of the genome associated with a killer disease.

Right, but as I was trying to say, probably not clearly enough, is that humans battle with chronic lymphocytic leukemia too, so while resistance to disease might be a good reason for the gene to be disabled in apes (though there's still the issue of the same mutation being involved each time), that should also be a good reason for it to be disabled in humans.

In the meantime you keep bringing up the point that the Duffy gene may only be independent in 2 populations and not 3, which frankly appears nitpicky.

Not really, it's a matter of exponential series: when something is very unlikely, having that something happen several times together gets very, very unlikely very, very fast, so the difference between 2 and 3 can be quite significant. Like for example if something has 1 in 10,000 chances of happening to someone we'd expect to see it happen twice to quite a few people worldwide (1 in 100,000,000 chance out of 7 billion people) but we wouldn't expect to see it happening to anyone three times (1 in 1,000,000,000,000 chance).
But at the end of the day given I don't know the specific probabilities here and haven't found out what the current ideas are on the origin of the two haplotypes I'm fine with letting that distinction drop.

I assumed you were a person who wants to make progress in these discussions and instead I have to re-explain my points and get distracted by side-issues. Your human/ape common descent argument is far from conclusive given ability of genes to mutate (and become selected) into non-coding regions in cases when a population is under threat from a deadly disease. The fact that even the original article you cited states that this gene is associated with a specific disease strengthens my point.

Before we go any further I would like you to acknowledge that your human/ape common descent argument is not conclusive, my points have sufficiently covered all your objections.

Given it doesn't seem to me you understood my objections I cannot do that, sorry. But it seems to me we've gone way off-track somewhere; I wasn't trying to convince you that the arguments were conclusive, and I apologize if I gave that impression or got carried away. Convincing you that the arguments were conclusive would be tantamount to convincing you of common descent which is a ridiculous goal for a single specific conversation and something I try to avoid.
As I said previously I brought up the article because you'd talked about how we only observe deteriorations in the genome and no improvements and I assumed you were referring to what scientists have observed, so I pointed out that the same scientists who observe deteriorations also think they're observing improvements, using the same basic assumptions. Once I'd said that it was natural to explain to you the arguments that they used and why they found them compelling. I was just trying to help you understand their point of view, I wasn't trying to convince you of their conclusions and if I slipped into acting like it in the course of the conversation I apologize.
I enjoy this discussion and would like to continue it, I'm willing to let all discussion of that article drop if that's not going anywhere and focus on other points. I will be sorry if you don't wish to continue at all but that is of course your right.

#96 NewPath

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Posted 26 June 2012 - 11:37 AM

Given it doesn't seem to me you understood my objections I cannot do that, sorry. But it seems to me we've gone way off-track somewhere; I wasn't trying to convince you that the arguments were conclusive, and I apologize if I gave that impression or got carried away. Convincing you that the arguments were conclusive would be tantamount to convincing you of common descent which is a ridiculous goal for a single specific conversation and something I try to avoid.


I see this process as trying to convince the other of our own position. It requires a uniquely open individual to be able to do that, normally tempers flare long before there is any open-mindedness. I'm happy to carry on discussing these issues but you are breaking up my posts into little bits and trying to disagree with nearly every sentence. Rather just discuss the main points and find points of agreement rather than contention. I will try to do so as well.

In the very first paragraph of your link concerning ape/human common descent it says the following:http://genome.cshlp....752.full#ref-15
The genes are not well characterized, but interestingly, one of them was first identified as an up-regulated gene in chronic lymphocytic leukemia

I personally found it very interesting that they mentioned this "aside" point right in the opening paragraph with no subsequent mention. I would not be surprised to find that Gibbons that suffer from this disease are coding in that particular sequence of genes. I actually strongly suspect that will be the case, not just because of my creationist assumptions, but because that is what the evidence is already hinting at. So we are agreed then that the link concerning "recent de novo" origin is not conclusive proof that the non-coding region came first, I'm happy with that. Neither was I trying to say that it HAD to be a coding region that became non-coding, I was just indicating their confident conclusions are not as conclusive as they think they are.

.

Right, but as I was trying to say, probably not clearly enough, is that humans battle with chronic lymphocytic leukemia too, so while resistance to disease might be a good reason for the gene to be disabled in apes (though there's still the issue of the same mutation being involved each time), that should also be a good reason for it to be disabled in humans.


Well I do not know of the effects of the other two differences in that sequence of genes. Maybe the other apes used to be PARTICULARLY susceptible to that disease because of their lack of the two differences found in humans, or maybe the two differences prevent the disabler taking hold in the human. Maybe humans have been unlucky not having that disabling mutation. Maybe the selective pressures FAVORING that function are greater than the selection pressures favoring the disabling of that function because of the differing lifestyles of humans compared to apes. My point is simple, de-coding mutations are common, they sometimes occur in the identical spot across different populations and I believe we do not know the exact statistical chances of it occurring. We could carry on for another twenty pages of algorythyms and mutation rates and comparing the statistical chances of 4 apes compared to 2 human populations getting a disabler.That argument will be inconclusive because quite simply there have not been enough genomes sequenced and so we do not know of the rates of non-coding mutations to be able to conclude an argument for all mammal species on earth. Why even go there if science hasn't yet enough information?

I don't get it, are you saying when the gene's active it causes chronic lymphocytic leukemia ?


This particular comment seemed to show a lack of understanding of the Duffy situation, and therefore the non-coding apes as well. You smoothly say in the post above that you already know all this, why then the stange question in your previous post? By this stage you should have known that the gene does not cause the disease, merely the de-activation of the gene's activity reduces the susceptibility, if you had taken the time to understand the comparison.

#97 aelyn

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Posted 26 June 2012 - 02:21 PM

I see this process as trying to convince the other of our own position. It requires a uniquely open individual to be able to do that, normally tempers flare long before there is any open-mindedness. I'm happy to carry on discussing these issues but you are breaking up my posts into little bits and trying to disagree with nearly every sentence.

Sorry, it's a formatting habit I got on Usenet and that isn't as appropriate for forums. I've been trying to cut down but I'll try harder.

In the very first paragraph of your link concerning ape/human common descent it says the following:http://genome.cshlp....752.full#ref-15
The genes are not well characterized, but interestingly, one of them was first identified as an up-regulated gene in chronic lymphocytic leukemia

I personally found it very interesting that they mentioned this "aside" point right in the opening paragraph with no subsequent mention. I would not be surprised to find that Gibbons that suffer from this disease are coding in that particular sequence of genes. I actually strongly suspect that will be the case, not just because of my creationist assumptions, but because that is what the evidence is already hinting at. So we are agreed then that the link concerning "recent de novo" origin is not conclusive proof that the non-coding region came first, I'm happy with that. Neither was I trying to say that it HAD to be a coding region that became non-coding, I was just indicating their confident conclusions are not as conclusive as they think they are.


The gene being up-regulated in chronic lymphocytic leukemia unfortunately doesn't say much about its actual function and its effects when it's regulated at its usual levels, that's probably why the authors didn't say much more than that. And wanting to find agreement is all fine and good but if I don't agree there's nothing fine about you unilaterally declaring that we do. If you're tired about arguing the point that's what "agreeing to disagree" is for. I'm fine with doing that here.

Well I do not know of the effects of the other two differences in that sequence of genes. Maybe the other apes used to be PARTICULARLY susceptible to that disease because of their lack of the two differences found in humans, or maybe the two differences prevent the disabler taking hold in the human. Maybe humans have been unlucky not having that disabling mutation. Maybe the selective pressures FAVORING that function are greater than the selection pressures favoring the disabling of that function because of the differing lifestyles of humans compared to apes. My point is simple, de-coding mutations are common, they sometimes occur in the identical spot across different populations and I believe we do not know the exact statistical chances of it occurring. We could carry on for another twenty pages of algorythyms and mutation rates and comparing the statistical chances of 4 apes compared to 2 human populations getting a disabler.That argument will be inconclusive because quite simply there have not been enough genomes sequenced and so we do not know of the rates of non-coding mutations to be able to conclude an argument for all mammal species on earth. Why even go there if science hasn't yet enough information?

The other differences are not in the gene that's involved in leukemia, and their effects are shown in the paper : they either cause the whole sequence not to code for anything at all (because of the lack of a start codon), or they make stop codons occur at an earlier point (always before the bit where the protein is coded in humans anyway). They have nice figures showing where the stop codons would be if you ignored the additional frameshifts (red box) and if you include them (yellow boxes); I'll attach the one for the second gene but the description of the figure is in the paper. Any one of those differences on its own would disable the gene as surely as the disabler does so they wouldn't prevent the disabler from taking hold in humans, nor would adding them to the disabler help with apes being particularly susceptible to the disease; you can't super-disable a gene (unless I am again misunderstanding what you meant by those arguments).

Attached File  genes_figure.jpg   335.47KB   2 downloads

Of course just because those specific objections don't work doesn't mean we can't find others, and if we assume that gibbons that have leukemia have a coding version of that gene, or we assume that other apes are particularly sensitive to it, or any other such assumption we have little to no evidence for, we can explain how those genes ended up as they did. And we can always think they were created the way they are. At the end of the day your a priori likelihood for common descent is so low that any alternate hypothesis, no matter how lacking in evidence, will be more likely to you; that's why you find the authors' arguments inconclusive and it's why I'm not trying to convince you otherwise. It's a perfectly reasonable position given your starting assumptions. I was hoping I could get you to appreciate why people who don't attribute an infinitely low a priori likelihood to common descent might come to a different conclusion, but even if I failed at that I think we did have an interesting in-depth discussion; I'm fine with letting it go at that.

This particular comment seemed to show a lack of understanding of the Duffy situation, and therefore the non-coding apes as well. You smoothly say in the post above that you already know all this, why then the stange question in your previous post? By this stage you should have known that the gene does not cause the disease, merely the de-activation of the gene's activity reduces the susceptibility, if you had taken the time to understand the comparison.

That comment showed a lack of understanding of what mechanism exactly you were positing with the first gene; I understood better after your response, hence the... lack of comment saying so, I must have edited it out before posting last time, okay then Posted Image
We'd been discussing the Duffy gene since long before that particular comment and we'd been going over the same things for some time, that's what I assumed you were talking about when you complained about it.

#98 NewPath

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Posted 26 June 2012 - 11:38 PM

Of course just because those specific objections don't work doesn't mean we can't find others, and if we assume that gibbons that have leukemia have a coding version of that gene, or we assume that other apes are particularly sensitive to it, or any other such assumption we have little to no evidence for, we can explain how those genes ended up as they did. And we can always think they were created the way they are. At the end of the day your a priori likelihood for common descent is so low that any alternate hypothesis, no matter how lacking in evidence, will be more likely to you; that's why you find the authors' arguments inconclusive and it's why I'm not trying to convince you otherwise. It's a perfectly reasonable position given your starting assumptions. I was hoping I could get you to appreciate why people who don't attribute an infinitely low a priori likelihood to common descent might come to a different conclusion, but even if I failed at that I think we did have an interesting in-depth discussion; I'm fine with letting it go at that.


You attribute an infinitely low a priori likelihood to creationism and therefore would rather believe an entire unique non-coding region somehow evolved into a uniquely functional set of genes unmatched elsewhere in the ape's genome. And only THEN activated in humans.

#99 NewPath

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Posted 27 June 2012 - 12:04 AM

The gene being up-regulated in chronic lymphocytic leukemia unfortunately doesn't say much about its actual function and its effects when it's regulated at its usual levels, that's probably why the authors didn't say much more than that.


My point was to indicate that chronic lymphocytic leukemia is associated with that gene, and mentioned in that article. These are the facts. The disabling of that gene immediately brings to mind the possibility that its a subsequent protection mechanism. This is an obvious possibility. You fail to see this as a statistically viable proposition even though mutations regularly disable genes. I find your detailed focus on side-issues distracts you from being open-minded to very simple points.

There is no requirement in nature that a beneficial mutation occurs across all species, not all humans in malaria areas have the disabled Duffy gene, and so your detailed response regarding my guesswork concerning why humans do not have the disabled lymphocytic leukemia gene is all irrelevant. It is curious why humans do not have it, but our lack of knowledge of this fact does not add much to your argument, despite the emphasis you have placed on this.

#100 aelyn

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Posted 27 June 2012 - 01:08 AM

You attribute an infinitely low a priori likelihood to creationism and therefore would rather believe an entire unique non-coding region somehow evolved into a uniquely functional set of genes unmatched elsewhere in the ape's genome. And only THEN activated in humans.

There's nothing particularly unbelievable about that. There are 4 possible base pairs, the human genome contains 3 billion base pairs, 98% of it noncoding (and noncoding doesn't mean non-functional, but 98% of the genome isn't regulatory either). Every single 3-base pair combination codes for an amino acid, an initiation site or a stopping site. The odds that there exist short strings of codons in there that correspond to a functional protein and are just lacking an ORF isn't low at all. If those had been very long genes it would be another story but in fact they're very very short.

I really don't see how we can go further with this, can't we go back to the other points we were talking about before discussing this article took over the whole conversation ?

(although I would still like to find out more about those gibbons with chronic lymphocytic leukemia, I still haven't been able to find anything on that, maybe you could give me google search terms with which to find out more if nothing else ?)




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