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#61 aelyn

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Posted 07 June 2012 - 07:15 AM

Changes WITHIN species have been observed, that doesn't mean that changes from Reptiles to Birds are supported by those observations.

I never said they did, in fact I didn't say a word about reptiles. I did say that "species" is a fuzzy concept but it isn't remotely fuzzy enough to include birds and reptiles in a single species, so the reptile/bird difference isn't that useful for distinguishing microevolution from macroevolution. Or at least it isn't if we take "microevolution" to mean "evolution within species", but you also included the concept of "organism type". If birds and reptiles are both organism types then maybe they're relevant to distinguishing microevolution and macroevolution. Is "Bird" or "Reptile" an organism type ?

You are attempting to make apples out of oranges. Its not logical nor is it scientific, its basically a blatant representation of bias, if ever I saw one.

Just FWIW, that kind of dig is why I don't reply to you much anymore. I try to avoid criticising the good faith, intelligence or reasoning skills displayed in the other side's arguments as much as I can, not because I don't sometimes think it but because I know both sides sometimes think it. What you do when you write this is make me upset, and force me to choose between responding to the attacks (which, given both sides think these things, would quickly devolve into a mud-slinging contest), or to ignore them and try to respond in the most reasonable good-faith-assuming way I can achieve, which takes up an inordinate amount of time and emotional energy. I know I am not perfect on this front either so I've avoided saying such things in the middle of a discussion with you, but since here I'm in a discussion with NewPath I figured I'd tell you how such comments make me react just for once. I won't bring it up again.

Perhaps you'd be better off considering the main thrust of my post.

The main thrust of your post is a very general statement about evolution, so no. I'm interested in discussing specifics a lot more than generalities. I'm having a fairly specific discussion with NewPath about novel genes and given neither of us is using quite the same definition of microevolution as you are (or so I guess from what I've seen NewPath say in another thread about marsupials), your input is interesting but not relevant to me. Replying to you was already a tangent which I only went on because I was hoping you'd characterise "organism type".

#62 gilbo12345

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Posted 07 June 2012 - 11:29 AM

1. I never said they did, in fact I didn't say a word about reptiles. I did say that "species" is a fuzzy concept but it isn't remotely fuzzy enough to include birds and reptiles in a single species, so the reptile/bird difference isn't that useful for distinguishing microevolution from macroevolution. Or at least it isn't if we take "microevolution" to mean "evolution within species", but you also included the concept of "organism type". If birds and reptiles are both organism types then maybe they're relevant to distinguishing microevolution and macroevolution. Is "Bird" or "Reptile" an organism type ?


2. Just FWIW, that kind of dig is why I don't reply to you much anymore. I try to avoid criticising the good faith, intelligence or reasoning skills displayed in the other side's arguments as much as I can, not because I don't sometimes think it but because I know both sides sometimes think it. What you do when you write this is make me upset, and force me to choose between responding to the attacks (which, given both sides think these things, would quickly devolve into a mud-slinging contest), or to ignore them and try to respond in the most reasonable good-faith-assuming way I can achieve, which takes up an inordinate amount of time and emotional energy. I know I am not perfect on this front either so I've avoided saying such things in the middle of a discussion with you, but since here I'm in a discussion with NewPath I figured I'd tell you how such comments make me react just for once. I won't bring it up again.


3. The main thrust of your post is a very general statement about evolution, so no. I'm interested in discussing specifics a lot more than generalities. I'm having a fairly specific discussion with NewPath about novel genes and given neither of us is using quite the same definition of microevolution as you are (or so I guess from what I've seen NewPath say in another thread about marsupials), your input is interesting but not relevant to me. Replying to you was already a tangent which I only went on because I was hoping you'd characterise "organism type".


1. You know full well what I was meaning and what you yourself was saying. You were attempting to define evolution as "evoltionary change as defined by "Biology"" which in itself includes variation as "proof" of evolution. I am correcting you in that this definition given by the establishment is patently wrong, hence you are to by using it.


2. I don't cave to guilt trips dude. As I clearly and simply explained using variation as a definition of evolution is patently illogical and unscientific, and therefore indicates ones own bias on the issue. If you wish to be called unbiased then follow what reality shows and not include assumptions, (which are based on bias), into the mix. As the main thrust of my post surmised, what we observe are small superficial changes within species, which even if extrapolated out still wouldn't derive a bird from a reptile, (no you didn't say this is merely an example). Hence to be unbiased you should follow what the evidence tells you, and the evidence says that variations are simply superficial changes. Until you have evidence to the contrary, the actual scientific position is that variation is not evolution, (in the context of evolution being the progression of one form of organism to another, as Darwin put in his book). If you wish to call change = evolution then you will need to define what "kind" of evolution you mean and not blur the meanings as to use evidence for one as evidence for the other, since there is a distinction, (as I have shown here).


3. That was meant as a call for you to debate the actual post, not nit-pick on something I may have written wrong. The main thrust of my post was supporting points to demonstrate how variations are not evolution. The fact that you responded without regarding these points shows that you'd wish to avoid the logic of this area.

#63 aelyn

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Posted 07 June 2012 - 12:34 PM

1. You know full well what I was meaning and what you yourself was saying. You were attempting to define evolution as "evoltionary change as defined by "Biology"" which in itself includes variation as "proof" of evolution. I am correcting you in that this definition given by the establishment is patently wrong, hence you are to by using it.

I do know full well what I myself was saying : I was pointing out to NewPath that the definitions he was using were different from those biologists use. I explicitly wasn't telling him to use the biologists' definitions, I was just making sure we were on the same page. And your view that evolutionary biologists don't get to define the terms of their own field is noted. We already had a ten-page debate over this months ago so I don't see the point of saying more on this.

3. That was meant as a call for you to debate the actual post, not nit-pick on something I may have written wrong. The main thrust of my post was supporting points to demonstrate how variations are not evolution. The fact that you responded without regarding these points shows that you'd wish to avoid the logic of this area.

You think you wrote "organism type" wrong ? It looked well-spelled to me. The fact that you wrote a post about definitions, that offered a definition, and then didn't respond to a request for some very basic clarification of that definition shows... nothing at all; maybe you were just too busy.

#64 Hawkins

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Posted 08 June 2012 - 12:52 PM

Whenever the "definition of kind/species" card is thrown out, you shall smell equivocation. Kind/species cannot be well defined in terms of DNA (or something better) simply because humans (human scientists) are lame and thus incapable of defining them at that level. It by no means says that we cannot distinguish a cat from a dog. Kind/species is a human consensus in grouping living organisms sharing common but distinguishable characteristics. We know cat is different from dog even genetically though we may not be able to present the difference at the genetic level due to the lameness of human knowledge at this stage.

It by no means says that we cannot base on the term species to discuss the variance between a bacteria and a cat.

Scientifically speaking, if you declare that (all) water dissolves into hydrogen and oxygen, you should be able to allow any third party to use any water even from Mars or Neptune to do the test to get the result. If not "water dissolves into hydrogen an oxygen" will be falsified. This is referred to as the falsifiability of science.

Similarly, if ToE hints implicitly if not explicitly that (all) species are a result of evolution from a single cell (or whatever simple life forms), it should be able to allow anyone to pick any species (cat, dog, rat, fish, bird....you name it) to test evolution from a single cell to its current state (kind/species is never an issue unless you try to argue equivocally).

#65 Hawkins

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Posted 08 June 2012 - 01:19 PM

The fallacy the evolutionists have to use all the times.

If I successfully did an experiment to allow a cat to evolve to a dog. The experiment is a success, I actually demonstrated how a dog evolved from a cat. The question is, does it mean that a cat must have evolved from a single cell?

The answer is no, you can't use a much simpler process as a proof for a much more complicated process. If you say yes, you have fallen for a fallacy. Similarly, if you do allow bacteria to evolved to something else, say, a virus. What valid implication does this mean?

Because bacteria evolved into a virus such that,
dog must have evolved from a single cell?
cat must have evolved from a single cell?
cow?
rat?
bird?
fish?
<make a full list please>

If such a conclusion can be drawn that "because becteria evolved into virus, mammal evolution has already been known to humans", then we must have known from the process of "bacteria turned into virus" that how a mammal organ (such as brain, heart, lung...) is formed. Can we draw conclusions like this?

On the other hand, if such a conclusion cannot be drawn. What conclusion can be drawn? That is, from the process of "becteria evolved into virus", evolution of what from what can be confirmed?

#66 AFJ

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Posted 10 June 2012 - 06:16 PM

Say it was possible to do this experiment with a much more complex organism, like a fruit fly. At the end of it however long it ran for, I wouldn't expect any of the final populations to be anything but fruit flies. Some of them might be a new species, not capable of interbreeding with any species in it's ancestory. These would still be fruit flies but a subset of the original species.

You claim to buy the store, but only have enough for gallon of milk. This prediction does not match the predictions of evolution--namely, that more complex, more intelligent species arose from that which was less complex, less intelligent. For instance, many of the soft bodied phylla in the cambrian finds are claimed to be a "radiation" of the major body plans. This is definitely an intuitive claim that the less complex was the ancestor of the more complex. http://www.astrobiol...ages/res4c.html

Otherwise you have no choice but to say that the beginning was started with many simultaneous and varied common ancestors, which matches the predictions of creationism.


Birds(feathered, winged, bipedal, endothermic (warm-blooded), egg-laying, vertebrate animals) are a modified subset of therapods. If some of the flightless birds today evolved to loose their wings they would still be birds, just a modified subset so a possible defnition of those would be: feathered, NON-winged, bipedal, endothermic (warm-blooded), egg-laying, vertebrate animals. Where a species 'comes from', it is just a modified subset of its ancestors.

Your first statement is an unsubstantiated assumption--a repeated mantra of acedemia. You have no principle of science by which natural selection COULD select anything but a fully developed wing. I think the history of the airplane is scientific enough to show us that those designs which did not succeed were many and did not continue. Yet you want us to believe that populations of theropods had "evolving" wings. They either had wings that worked, or they did not have wings, for if natural selection is held to it's principle, then it will select that which is advantageous for the species. WHAT MAJOR DESIGN FEATURES COULD EVOLVE INCREMENTALLY WHICH WOULD BE USEFUL, AND A PRECURSOR OF A WING--BUT NOT BE A WING?



I highly doubt any evolutionary biologist would claim that. If the bacteria became aphids/lice/something other than bacteria this would invalidate the ToE.

So then aphids and lice came from an unknown common ancestor that is shown on the phylogenic tree as a branch. Because bacteria are SO different genetically from eukaryotes, they are given a seperate domain-- different tree. So since you seem to be advocating that evolution simply involves speciation, would you suppose that lice and aphids arose/descended from similarly designed ancestors? If so, then you are somewhat in agreement with creationism.

#67 NewPath

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Posted 11 June 2012 - 02:14 AM

http://genome.cshlp....19/10/1752.full

ps @ aelyn

I have to admit that I didn't read your links in detail, but now when looking into these new coding human genes compared to apes, very fascinating article!

And seemingly convincing until you look into the detail. There are many differences between the two genomes but they managed to find three differences where the the sequence is the same, the sequence is unique to hominids, yet the ape's genes appear to be non-coding, and the human's appear to be coding. The obvious evolutionary assumption is that in fact non-coding sequences can then become coding, adding to the complexity of what is known as the more complex human genome.

But if you think about it, their conclusion is based on the assumption of complexity over time. Evolution. If they had assumed "devolution" instead of evolution, the other possible conclusion would have been obvious too, the apes had previously coding regions which have since gone dead. ie they were both designed with an identical region, (most DNA of chimp/human is identical) but the chimp has since lost functionality in that region. This is confirmed by the fact that the apes (chimp and macaque) both had a disabler in the genes, which indicates coding genes thereafter becoming non-coding, rather than non-coding genes becoming coding. Devolution rather than evolution.http://genome.cshlp....752.full#ref-15

To conclude that the ape "devolved" from a human is not correct either, the ape could be devolving from its original chromosomal pattern, but both started off with differences that already existed.

#68 NewPath

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Posted 11 June 2012 - 05:42 AM

I now have, and no I don't see that at all. As you pointed out in your previous post they focus very much on the genes and their interactions, not their effect on the organism, and all the references I've seen to function in that paper are about the genes. In fact in the He and Zhang paper they quote as a reference for "subfunctionalization" which you kindly linked to, they define the concept this way :
Not only does that not refer to the organism's functionality at all, it's implied it would remain the same under that hypothesis since the activity of the duplicates would be "equivalent to" that of the progenitor gene.


Ok I get you here, but this subfunctionalisation does not add to your point. This is the "hypothesis" of subfunctionalisation (SF) , which basically means its a theory without evidence.

I tried to understand the article, how I see it, when testing for function , they did attempt to prove a hybrid of the SF and the NF (neofunctionalisation) hypotheses. However their test of function basically related to "basic activity" within a gene, protein-protein interaction. They initially measured rapid SF which is basically means rapid distribution of the original functions among more genes. They do not say whether this resulted in more or less fitness for the organism, just that the original functions are distributed. They then based their evidence of new functions (NF) on the evidence of protein-protein interaction in the new genes. Which isn't really saying anything more than the original SF theory, they are just saying that protein-protein interaction is NF, I don't see that as new functions, it just points to some activity in the new genes and does not point to the organism or genes having new functions at all.

In summary , it just seems like the duplications are sometimes creating active genes, which is always apparent in Down's syndrome. This does not mean the organism will die, but it could lose some functions while gaining extra active genes just like Down's syndrome.



I'm sorry, these two statements back-to-back confuse me. A) You say the genome differences between humans and chimpanzees are "too significant" to be explained by what we currently know of mutations; which genome differences are you thinking of specifically ?
B) And then you say that "looking at the evidence it looks like things are deteriorating fast, and with no evidence for 'extra functional genes'; are you still referring to the human and chimpanzee genomes ?


A) I am referring to the chimp having extra useful coding genes in chromosomes 2,8,13,14,17,18,20,21,22 and the human having extra genes in chromosomes 1.9,Y
B) I am referring to ERV's, duplications, damaging mutations, deletions etc


It is ? I figured I'd check Wikipedia just to make sure, and it seems the researchers involved do think a gene duplication + mutation was involved (whether this was a frameshift mutation or base substitution seems to be what people disagree on).


A frameshift mutation or a base substitution are BOTH mutations within a gene, not an added or deleted gene.


But what I was going to ask before I checked Wikipedia and saw people think it's an extra gene after all, was : we seem to agree genes can change. We seem to agree they can change towards useful functions, if you do think nylon eating bacteria are an example of a changed gene. We also agree genes can duplicate.


I agree genes can change, I agree genes can change usefully. I do not agree that an EXTRA gene can change beneficially. Extra genes that are activated, protein coding, cause damage (Down's syndrome). Deleted genes or chromosomes can occasionally have a limited benefit even while losing functionality (Duffy gene), but most deleted genes cause mutational damage, all added coding genes cause damage or are neutral without a benefit.


So I wonder, what's stopping extra genes from developing ? I'm not talking about every duplicate mutating into a beneficial extra gene here. But there are tons of duplications. Even if, say, 99.9% of duplicated genes deteriorate or become harmful, there are thousands of genes, millions of base pairs, and every species contains hundreds or thousands or more individuals every generation, and lasts for quite a few generations. On a purely statistical basis, extra beneficial genes have to develop. Now if 100% of duplicated genes deteriorate or become harmful they can't... but how do we justify that percentage when we know that some genes are beneficial, and we know from nucleotide-by-nucleotide comparisons that many of them are only a few base pairs or frameshifts away from a non-coding stretch of DNA or a less-effective gene ? What is stopping one duplicate gene in a million from changing its function, or one stretch of noncoding DNA in a billion from becoming coding ? Or regulatory ?


Maybe a higher power created intelligent genes, and nature is unable to combine 100 000 base pairs to add any significant extra function naturally (ie nature cannot generate highly technical biological matter on its own). This limits the creation of intelligent improvements to organisms.

#69 NewPath

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Posted 12 June 2012 - 04:43 AM

Except that isn't current observation. I mean, you can disagree with the methods or conclusions of the scientists looking into genetics, but [i]they think they're also seeing evidence of gene creation, coding regions developing from noncoding ones, deletions and disabling mutations that result in unchanged or improved function, and so on. I'm not a geneticist; if I believe geneticists when they say they see gene losses and deterioration why shouldn't I also believe them when they say they see gene gains and improvements ?

Because they do not claim an extra coding (non-viral) gene can benefit the entire organism through improved fitness and therefore improved natural selection. Do they claim this ?? (Maybe I missed something in those studies you posted). The study claiming extra functional genes was not claiming those genes are improved or that the organism is improved. Their measure of gene functionality was "protein-protein interaction". Even cancers have protein-protein interaction, maybe those new genes are cancerous? The study concerning nylon was referring to indels within a gene, not an extra gene. One E coli experiment concerned an artificially inserted "cloned gene" that added hardiness but not extra coding to the organism. So I'm yet to see your claims of extra coding genes benefiting the organism. Please re-post any links I may have missed in case I did miss something :)

wikipedia:
Interactions between proteins are important for the majority of biological functions. For example, signals from the exterior of a cell are mediated to the inside of that cell by protein–protein interactions of the signaling molecules. This process, called signal transduction, plays a fundamental role in many biological processes and in many diseases (e.g. cancers)

#70 aelyn

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Posted 12 June 2012 - 12:08 PM

http://genome.cshlp....19/10/1752.full

ps @ aelyn

I have to admit that I didn't read your links in detail, but now when looking into these new coding human genes compared to apes, very fascinating article!

And seemingly convincing until you look into the detail. There are many differences between the two genomes but they managed to find three differences where the the sequence is the same, the sequence is unique to hominids, yet the ape's genes appear to be non-coding, and the human's appear to be coding. The obvious evolutionary assumption is that in fact non-coding sequences can then become coding, adding to the complexity of what is known as the more complex human genome.

But if you think about it, their conclusion is based on the assumption of complexity over time. Evolution. If they had assumed "devolution" instead of evolution, the other possible conclusion would have been obvious too, the apes had previously coding regions which have since gone dead. ie they were both designed with an identical region, (most DNA of chimp/human is identical) but the chimp has since lost functionality in that region. This is confirmed by the fact that the apes (chimp and macaque) both had a disabler in the genes, which indicates coding genes thereafter becoming non-coding, rather than non-coding genes becoming coding. Devolution rather than evolution.http://genome.cshlp....752.full#ref-15

To conclude that the ape "devolved" from a human is not correct either, the ape could be devolving from its original chromosomal pattern, but both started off with differences that already existed.


Actually their conclusion isn't based on the assumption of increased complexity over time, and they did consider the possibility that the genes had originally been coding and got deactivated in non-human apes; it's not an issue of evolution vs devolution, it's the fact that mutation is a reversible process, i.e. it has no inherent direction. Two similar sequences could have evolved from each other but you can't tell which one is ancestral just from looking at them.

As they explain in the article they dismiss that possibility because the non-coding sequences are non-coding in the exact same way in the other ape species. If the coding sequence had been ancestral and every ape species other than humans had lost it then they wouldn't all have lost it in the exact same way. The other alternative is that the nested hierarchy of apes is wrong and that all apes share a more recent common ancestor with each other than they do with humans, but the balance of the evidence for the existing hierarchy is too strong to give that hypothesis much credence either.

So their conclusion isn't based on the assumption that complexity increases, but on the assumption that the current classification of apes isn't utterly wrong.

There is also the possibility that the gene was active in an ancestor to apes, became deactivated in the common ancestor of all apes, and was reactivated in humans. This is also unlikely given they say they couldn't find any equivalent to those genes in "any sequenced genome". I don't know how many genomes have been sequenced by now but I think it's a lot.

Which isn't really saying anything more than the original SF theory, they are just saying that protein-protein interaction is NF, I don't see that as new functions, it just points to some activity in the new genes and does not point to the organism or genes having new functions at all.

Fair enough. As I said when I linked to the article in the first place I was offering it as an example of duplicated genes having "real genetic effects" without having changed much otherwise. How significant you feel those effects are is up to you, and certainly it's the kind of short-term effect that isn't the most relevant aspect of long-term evolution anyway.

In summary , it just seems like the duplications are sometimes creating active genes, which is always apparent in Down's syndrome. This does not mean the organism will die, but it could lose some functions while gaining extra active genes just like Down's syndrome.

I'm not sure what you mean by "extra active genes" here. I'd been assuming that duplicates didn't count as "extra" genes, but duplicates are all that Down's syndrome generates. (well, maybe individual people with Down's syndrome might have mutations in chromosome 21 that would make some of the duplicate genes different, but it's not relevant to the syndrome as a whole, which is just about having the extra chromosome)

A) I am referring to the chimp having extra useful coding genes in chromosomes 2,8,13,14,17,18,20,21,22 and the human having extra genes in chromosomes 1.9,Y

And with all of those genes we can count and name the nucleotide substitutions that make them differ, can't we ? AFAIK it's by comparing human and chimpanzee genes nucleotide by nucleotide that we found those differences in the first place. Nucleotide substitution is one kind of currently observed point mutation. Why couldn't such mutations and selection over many generations build up this kind of difference ?

B ) I am referring to ERV's, duplications, damaging mutations, deletions etc

Of course these are also found by comparing genomes nucleotide by nucleotide - I don't think we've ever caught an ERV in the process of introducing itself into a live human's genome. Geneticists look at genes, and find that some of them look exactly like virus genomes, or look like each other as if they'd been duplicated, or look just like the functional genes of another species except with small differences that make them non-functional, etc.
Given point mutations are a completely reversible process, why is it that when you look at two similar genes, one functional and one inactivated, you readily accept that a mutation inactivated one of them but you think it's impossible that the opposite mutation could have activated the other ? (there are actually good thermodynamic reasons why one would be less likely than the other, but for one thing selection changes the picture, and for another it seems to me you're making a much stronger argument than mere unlikelihood)

A frameshift mutation or a base substitution are BOTH mutations within a gene, not an added or deleted gene.

You missed the "duplication" bit of "gene duplication + mutation was involved". In fact the "duplication" bit is the only thing everyone seems to agree on given the paper I read.

I do not agree that an EXTRA gene can change beneficially. Extra genes that are activated, protein coding, cause damage (Down's syndrome). Deleted genes or chromosomes can occasionally have a limited benefit even while losing functionality (Duffy gene), but most deleted genes cause mutational damage, all added coding genes cause damage or are neutral without a benefit.

Well, Down's syndrome is an added chromosome. That's a completely different order of magnitude from an added gene. That said, even adding chromosomes isn't always bad, with plants being the typical example. It's true this is very group-specific, mammals don't take to polyploidy like plants or even fish do, but it seemed to me your statements included all of eukaryotes, not just mammals.
That said, I am still wondering about this. You say you agree a gene can change beneficially, and you also say that added coding genes can be neutral. Can neutral genes change beneficially ? Can an added coding gene that's neutral, later change beneficially ? As I see it there are two ways this could be impossible : if there were an additional process keeping it from happening, or if the odds of it happening were so small that it would never happen in practice.
If it's the first one, do you have details on what the additional process is ? If it's the second, how did you calculate those odds ? (I don't suppose you have actual numbers of course, but just understanding your thought process would be fine by me)

Maybe a higher power created intelligent genes, and nature is unable to combine 100 000 base pairs to add any significant extra function naturally (ie nature cannot generate highly technical biological matter on its own). This limits the creation of intelligent improvements to organisms.

That doesn't answer my question at all : you're basically saying "maybe it's impossible for new genes to arise" (I'm not completely sure what "highly technical biological matter" means, but as this has all been about new genes up to now I'll assume that's what you mean). But the basic processes for new genes arising are all there. Statistically speaking, new genes would have to arise once in awhile, if all the genetic processes we agreed happen do happen. It could very well be impossible for it to happen, but that would require an additional process at work.

Kind of like, statistically speaking harmful mutations have to dramatically outweigh the beneficial ones (because given organisms already work quite well it's much easier for things to go wrong than for things to improve). We can't wave our hands and say "but beneficial ones happen too, so if they add up then adaptation can happen". No it can't. You can't escape statistics when you're talking about huge numbers, and all the genes in all the organisms over all the generations is a huge number. To have beneficial mutations add up and outweigh the harmful mutations we either have to be wrong on the basic genetics, or we need an additional process. And we do have one : natural selection. Harmful mutations lead to the organism bearing them to not reproduce, and so even though those mutations happened, they don't spread to the next generation. Beneficial mutations on the other hand, do. Thus, while the process of mutation alone would not lead to adaptation, the processes of mutation and natural selection together can.

So here it's the same thing. As far as I can tell, new genes are an inevitable consequence of how genetics work. For them to be impossible you need an additional process that keeps them from arising. I'm fine with the answer "higher power", I just find it strange that a higher power would create genetic processes that make the formation of new genes inevitable, and would then actively stop those new genes from forming.

Because they do not claim an extra coding (non-viral) gene can benefit the entire organism through improved fitness and therefore improved natural selection. Do they claim this ??

They certainly claim this for the Human Accelerated Regions of the human genome. And I'm sorry but I'm going to completely shrug off your requirement that the new genes be protein-coding for that particular example because I think that a genetic change that could lead to our high intelligence is a lot more important than some measly protein. But as for proteins, the researchers who say they found the new protein-coding CG11700 gene in drosophilas also think it's functional, namely that regulates a trade-off between male fecundity and lifespan in a way that doesn't happen in flies that don't have that gene. I'm not sure which study you're referring to concerning nylon, I was talking about the one by Negoro et al 2007, which say in the introduction "These results suggest that the EII has evolved by gene duplication followed by base substitution from its ancestral gene."

Finally, although I've been too busy to post lately I've still been looking at the forum now and then, and I seemed to recall some other arguments by you that I can't find here. Given you've made several posts during that time I figure you might also have edited your posts, or I'm just remembering wrong. If I did miss one of your replies please tell me :)

#71 joman

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Posted 12 June 2012 - 10:35 PM

Kind begets kind.

That is the law of multiplication of offspring.
There are no known exceptions.

Variation within kind promotes survival of the kind and has a rational purpose.
Variation within a kind has not proven to be macro-evolutionary.

The concept of macro-evolution has no rational purpose, however.

For, a purposeless maco-evolutionary change would be an unatural result within a already naturally balanced eco system and habitat.
New and advantaged creatures would by definition not naturally fit, have proper form, nor appropriately function within the existing balance of nature because, natural selection criteria for a particular kind would not include balance criteria factors favoring the survival needs of other kinds of creatures.

This means that purposeless macro-evolutionary change due to natural selection for the benefit of a particular kind of creature naturally trends against the natural balance of the larger system of many kinds, and thus leads to destruction of the larger system of nature.

This also applies to somatic cells that are supposed to be allowed to macro-evolve in favor of itself and in disfavor of the body whole.
That is, the concept of purposeless macro-evolutionary change is best expressed by cancerous growth.
If a variation doesn't fit it won't function.
If a variation has the wrong form it can't fit, nor function.
If a variation is the wrong function it is useless.

And so the limits to variation within kind are necessary for survival.

#72 NewPath

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Posted 13 June 2012 - 12:55 AM

Actually their conclusion isn't based on the assumption of increased complexity over time, and they did consider the possibility that the genes had originally been coding and got deactivated in non-human apes; it's not an issue of evolution vs devolution, it's the fact that mutation is a reversible process, i.e. it has no inherent direction. Two similar sequences could have evolved from each other but you can't tell which one is ancestral just from looking at them.

As they explain in the article they dismiss that possibility because the non-coding sequences are non-coding in the exact same way in the other ape species. If the coding sequence had been ancestral and every ape species other than humans had lost it then they wouldn't all have lost it in the exact same way. The other alternative is that the nested hierarchy of apes is wrong and that all apes share a more recent common ancestor with each other than they do with humans, but the balance of the evidence for the existing hierarchy is too strong to give that hypothesis much credence either.

So their conclusion isn't based on the assumption that complexity increases, but on the assumption that the current classification of apes isn't utterly wrong.

There is also the possibility that the gene was active in an ancestor to apes, became deactivated in the common ancestor of all apes, and was reactivated in humans. This is also unlikely given they say they couldn't find any equivalent to those genes in "any sequenced genome". I don't know how many genomes have been sequenced by now but I think it's a lot.


You admit the possibility that the gene was active and then became de-activated. I would have to look at the genome sequencing of both apes to see if they are in fact two sub-species or not, until then its possible that they are. Let me tell you about the Duffy gene, Malaria affects humans in which this gene is active. Every now and then a human mutates a "dead gene" somewhere. This dead Duffy gene became simultaneously prolific in two separate populations due to Malaria in each area. Which proves that two separate species or subspecies with similar genomes can have the same mutation becoming prolific in the population if that mutation has similar benefits across both species (eg a disease affecting apes and not humans). Thus it looks like the apes had reduced functionality and the humans retained functionality in that area of the genome.

To summarise
1) as you say, the two apes could be recent sub-species and that is why they show identical subsequent non-coding regions
2) They both have the same disabler (indels) which definitely points to subsequent non-coding, they wouldn't call the disabler an indel if it was already there.
3) They could both have independently gained non-coding regions in the same place because of the same environmental pressures on both types of apes as can be seen in the human Duffy gene.

So you have brought up a good point, but unfortunately it does not conclusively support your position, too many alternative interpretations of the evidence.


Fair enough. As I said when I linked to the article in the first place I was offering it as an example of duplicated genes having "real genetic effects" without having changed much otherwise. How significant you feel those effects are is up to you, and certainly it's the kind of short-term effect that isn't the most relevant aspect of long-term evolution anyway.


Yes duplications can have advantages, normally in hardiness , but not complexity. These are significant enough, but not in the debate concerning evolution as the source for complex life-forms, the theory that involves more and more important coding genes being added to the genome.

I'm not sure what you mean by "extra active genes" here. I'd been assuming that duplicates didn't count as "extra" genes, but duplicates are all that Down's syndrome generates. (well, maybe individual people with Down's syndrome might have mutations in chromosome 21 that would make some of the duplicate genes different, but it's not relevant to the syndrome as a whole, which is just about having the extra chromosome)


Down's syndrome produces extra proteins, i assumed because the duplicates are active. Either way, I suppose the syndrome points to additional activity to the norm being destructive. I feel this is generally observable.



And with all of those genes we can count and name the nucleotide substitutions that make them differ, can't we ? AFAIK it's by comparing human and chimpanzee genes nucleotide by nucleotide that we found those differences in the first place. Nucleotide substitution is one kind of currently observed point mutation. Why couldn't such mutations and selection over many generations build up this kind of difference ?


I call that interesting speculation. Sure it may be possible but never observed. In the meantime its appears impossible for nature to create new active genes. To base the whole theory of the complexity of life on a hypothesis that maybe extra genes can activate seems unscientific to me. It looked ok to Darwin because he observed changes, and he made sense. Since then we have seen that extra active genes are required and now we do not observe changes in these so the theory of evolution has lost strength with the introduction of molecular biology. The ability to get significantly complex appears restricted.

Of course these are also found by comparing genomes nucleotide by nucleotide - I don't think we've ever caught an ERV in the process of introducing itself into a live human's genome. Geneticists look at genes, and find that some of them look exactly like virus genomes, or look like each other as if they'd been duplicated, or look just like the functional genes of another species except with small differences that make them non-functional, etc.
Given point mutations are a completely reversible process, why is it that when you look at two similar genes, one functional and one inactivated, you readily accept that a mutation inactivated one of them but you think it's impossible that the opposite mutation could have activated the other ? (there are actually good thermodynamic reasons why one would be less likely than the other, but for one thing selection changes the picture, and for another it seems to me you're making a much stronger argument than mere unlikelihood)


The reason I assume this is that we do know that de-activations are favorable. We do not observe a human population with an extra coding gene in an isolated region showing favorable selective pressure. Yet in the laboratory and in nature we have many instances of favorable mutations involving de-activation of a gene. Thus the one process is more observed than the other process which is completely unobserved. Thus when we come across a section of the genome that is identical in two species yet the one is activated and the other de-activated its not logical to write a paper claiming proof of evolution. Its better to remain neutral , not assuming proof of evolution, and if any assumption is made it should be based on the more proven observed process than the less proven unobserved process. (there is currently a statistical bias towards devolution rather than evolution, some instances of devolution are absolutely proven (dead genes being beneficial), yet no instances of new active protein coding genes are proven to be beneficial to an organism).


You missed the "duplication" bit of "gene duplication + mutation was involved". In fact the "duplication" bit is the only thing everyone seems to agree on given the paper I read.

Will look at the link again and answer this in a following post.

Well, Down's syndrome is an added chromosome. That's a completely different order of magnitude from an added gene. That said, even adding chromosomes isn't always bad, with plants being the typical example. It's true this is very group-specific, mammals don't take to polyploidy like plants or even fish do, but it seemed to me your statements included all of eukaryotes, not just mammals.
That said, I am still wondering about this. You say you agree a gene can change beneficially, and you also say that added coding genes can be neutral. Can neutral genes change beneficially ? Can an added coding gene that's neutral, later change beneficially ? As I see it there are two ways this could be impossible : if there were an additional process keeping it from happening, or if the odds of it happening were so small that it would never happen in practice.
If it's the first one, do you have details on what the additional process is ? If it's the second, how did you calculate those odds ? (I don't suppose you have actual numbers of course, but just understanding your thought process would be fine by me)


You seem to make a good point here, but the reality is that the neutral gene cannot change and activate beneficially. To put this into simplistic terms, imagine a secret code that is designed to produce a foot. Duplicate it. No problem, the duplication is inactive. Activate it. Now you have three feet with two legs. BIG problem. The same applies to subtle things like heart speed, it must go with the right size of body, correct heart muscles, veins that can handle blood flow. I don't know much about biology but can you see the problems when you duplicate an active gene without redesigning the entire organism at the same time? Even if you mutate the active gene, much of that gene will still retain the original function and you would have a problem with the activated duplicate duplicating a lot of the functions of the original. Duplicates are good as "backup systems", not as active genes.

Kind of like, statistically speaking harmful mutations have to dramatically outweigh the beneficial ones (because given organisms already work quite well it's much easier for things to go wrong than for things to improve). We can't wave our hands and say "but beneficial ones happen too, so if they add up then adaptation can happen". No it can't. You can't escape statistics when you're talking about huge numbers, and all the genes in all the organisms over all the generations is a huge number. To have beneficial mutations add up and outweigh the harmful mutations we either have to be wrong on the basic genetics, or we need an additional process. And we do have one : natural selection. Harmful mutations lead to the organism bearing them to not reproduce, and so even though those mutations happened, they don't spread to the next generation. Beneficial mutations on the other hand, do. Thus, while the process of mutation alone would not lead to adaptation, the processes of mutation and natural selection together can.


Well said, i agree with the logic. However I get the impression that damage to genomes is accumulating faster than natural selection can deselect it. there are many genetic diseases in humans that should have been de-selected. The fact that damages can have permanent benefits "Duffy gene" also indicates damage rather than improvement over time. Necessary damage because of changing environments, but damage nevertheless.


So here it's the same thing. As far as I can tell, new genes are an inevitable consequence of how genetics work. For them to be impossible you need an additional process that keeps them from arising. I'm fine with the answer "higher power", I just find it strange that a higher power would create genetic processes that make the formation of new genes inevitable, and would then actively stop those new genes from forming.


I believe the balance of evidence at the moment is pointing to the sudden appearance of already advanced life-forms. (the evidence being the difficulty to create new good active genes). Thus no new genes are needed, You seem to think that evolving should occur anyway. Its absolutely unnecessary if the design was good in the first place. Yes the number of allele combinations is multiple trillions times by multiple trillions so the ability for each creature to adapt to its environment is already there, but you do not need more than that with well designed creatures.


The so-called ability of new beneficial genes being formed is just a mental projection of evolutionists, you seem to think your logic makes this possible and necessary, I still say impossible and unnecessary. Activate a new gene and you cause damage, I explained how above.



They certainly claim this for the Human Accelerated Regions of the human genome. And I'm sorry but I'm going to completely shrug off your requirement that the new genes be protein-coding for that particular example because I think that a genetic change that could lead to our high intelligence is a lot more important than some measly protein. But as for proteins, the researchers who say they found the new protein-coding CG11700 gene in drosophilas also think it's functional, namely that regulates a trade-off between male fecundity and lifespan in a way that doesn't happen in flies that don't have that gene. I'm not sure which study you're referring to concerning nylon, I was talking about the one by Negoro et al 2007, which say in the introduction "These results suggest that the EII has evolved by gene duplication followed by base substitution from its ancestral gene."


Again were those HAR regions designed or created like that ? Its hard to tell when we just know its there already. Yes there's other aspects important to evolution but I still want to focus on the necessary process of adding extra good protein-coding genes so I do feel that's a distraction.

The CG11700 gene, haha cleverly worded! You say it developed a trade-off between male fecundity and lifespan. Only the NULL mutants developed the trade-off, the OVEREXPRESSED CG11700 dropped fecundity without any life-span trade-off. It appears neither the null or the overexpressed CG11700 had an overall benefit to the organism, "trade-off" indicating as much damage as benefit.

"Null mutants ofCG11700 have a higher male fecundity but shorter lifespan, whereas its overexpression decreases male fecundity"

And so once again your example cannot explain the increase of favorable CODING genes claimed by evolution whereby life gets more complex over time. Sure trade-offs can occur with non-coding duplicate genes, but this fails to explain the mechanism by which humans evolved from bacteria.

Finally, although I've been too busy to post lately I've still been looking at the forum now and then, and I seemed to recall some other arguments by you that I can't find here. Given you've made several posts during that time I figure you might also have edited your posts, or I'm just remembering wrong. If I did miss one of your replies please tell me :)


I deleted one post when I realised I was replying to your same post twice, maybe that's it. If you describe what I said we could talk about it, but I think we have enough to go on, and I like to keep narrowing the conversation to a conclusion rather than increasing discussion topics, which can get impossible to deal with.

#73 aelyn

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Posted 13 June 2012 - 05:00 AM

You admit the possibility that the gene was active and then became de-activated. I would have to look at the genome sequencing of both apes to see if they are in fact two sub-species or not, until then its possible that they are.

When you say "both apes", are you referring to the non-human apes whose genomes were looked at in the study ? If so you should have looked at it before responding. Quoting from the abstract : "Furthermore, chimp, gorilla, gibbon, and macaque share the same disabling sequence difference, supporting the inference that the ancestral sequence was noncoding over the alternative possibility of parallel gene inactivation in multiple primate lineages."
Please don't tell me you're saying it's possible that chimps, gorillas, gibbons and macaques are sub-species of one another :)
(If you are saying that I'd have to ask what definition of "sub-species" you're using, and why humans don't belong to that species too)

Let me tell you about the Duffy gene, Malaria affects humans in which this gene is active. Every now and then a human mutates a "dead gene" somewhere. This dead Duffy gene became simultaneously prolific in two separate populations due to Malaria in each area. Which proves that two separate species or subspecies with similar genomes can have the same mutation becoming prolific in the population if that mutation has similar benefits across both species (eg a disease affecting apes and not humans). Thus it looks like the apes had reduced functionality and the humans retained functionality in that area of the genome.

The odds of the same mutation happening in two different populations is low, but not so low it's impossible (especially when accounting for mutation hot spots) (although it's low enough that I'd be interested in a cite for the claim the Duffy gene became "dead" in the exact same way in two independent populations). But those odds go down dramatically every time you add a mutation, and every time you add a population that purportedly got this mutation independently. Here we're talking about several mutations in four different lineages. The odds are easily in the "negligible" range.

Could you kindly acknowledge this possibility of de-activation rather than activation , you seem to have already acknowledged this in the bolded portion and if the genomes are extremely similar you could be right about these being relatively recent sub-species. I have no problem with that but would have to look at the genome.

Of course I acknowledge this possibility, as you point out I acknowledged it in my response to you, and not only in the bolded portions either (that paragraph about mutations being reversible and us not being able to tell which way they'd gone just from looking at two genes ? That was a direct statement that it could have been a de-activation).
Can we agree that the authors of the paper also acknowledged this possibility and made substantive arguments for why they dismissed it ?

I call that interesting speculation. Sure it may be possible but never observed. In the meantime its appears impossible for nature to create new active genes. To base the whole theory of the complexity of life on a hypothesis that maybe extra genes can activate seems unscientific to me.

Is it interesting speculation that Pluto orbits the Sun ? Such an orbit has never been observed. For that matter, until last year such an orbit of Neptune had never been observed either. The creation of a new gene hasn't been observed from beginning to end, but "hasn't been observed" and "appears impossible" are two completely different things. Given everything we've agreed upon about how genes work, the creation of new active genes doesn't only appear possible, it appears to be inevitable. I understand you disagree with this but I'd like to have an argument as to why this isn't true. "We haven't observed it therefore it's impossible" doesn't work.

I'm also a bit confused by your use of "activate". Maybe you mean "being expressed" ? But we do know of duplicate genes being expressed, the papers we've been discussing are full of examples. And whether a gene is expressed or not depends purely on its nucleotide sequence and the nucleotide sequence of the DNA around it, so changing a gene's expression and changing the nucleotide sequence of a stretch of DNA is the same thing.

The reason I assume this is that we do know that de-activations are favorable. We do not observe a human population with an extra gene in an isolated region showing favorable selective pressure. Yet in the laboratory and in nature we have many instances of favorable mutations involving de-activation of a gene. Thus the one process is more observed than the other process which is completely unobserved. Thus when we come across a section of the genome that is identical in two species yet the one is activated and the other de-activated its not logical to write a paper claiming proof of evolution. Its better to remain neutral , not assuming proof of evolution, and if any assumption is made it should be based on the more proven observed process than the less proven unobserved process. (there is currently a statistical bias towards devolution rather than evolution, some instances of devolution are absolutely proven (dead genes being beneficial), yet no instances of new active protein coding genes are proven to be beneficial to an organism).

Nobody today is writing papers claiming proof of evolution; in biology evolution is considered a proven fact (well, the basics of it at least). Of course creationists don't think it's proven, I'm just saying that's the state of the field. The paper we're talking about certainly didn't claim proof of evolution. They were claiming proof that new genes formed in humans from noncoding DNA. Again, I realize that you consider "new genes forming" and "evolution" to be synonymous, but to biologists "new genes forming" is just one aspect of evolution, and that's what the paper was looking at.
Now you are absolutely right that damaging mutations are much more common than beneficial ones, so that when we look at two almost-identical genes, one functional and the other one not, the most likely scenario is that the non-functional one comes from the functional one. One can't just assume that the functional one came from the non-functional one and is an example of a new gene. But two things : first, this is not what the geneticists who claim to find new genes do. They have actual arguments why they think they've found a new gene, and you should address those instead of mischaracterizing their position as "claiming proof of evolution" just because they "came across a section of the genome that is identical in two species yet the one is activated and the other de-activated".
And second, while it is true it is less likely for a mutation to turn a noncoding stretch of DNA into a gene rather than the opposite, your argument is much stronger than that : you are saying it's impossible. That argument is what I would like you to justify.

You seem to make a good point here, but the reality is that the neutral gene cannot change and activate beneficially.

Why not ? Please give arguments for this, don't just assert it. Or should I say, given what comes next, please give arguments that are based in how genes actually work.

To put this into simplistic terms, imagine a secret code that is designed to produce a foot. Duplicate it. No problem, the duplication is inactive. Activate it. Now you have three feet with two legs. BIG problem. The same applies to subtle things like heart speed, it must go with the right size of body, correct heart muscles, veins that can handle blood flow. I don't know much about biology but can you see the problems when you duplicate an active gene without redesigning the entire organism at the same time? Even if you mutate the active gene, much of that gene will still retain the original function and you would have a problem with the activated duplicate duplicating a lot of the functions of the original. Duplicates are good as "backup systems", not as active genes.

I'm sorry but this isn't how genes work at all. For one thing, there is no reason the duplication would be "inactive" to start with. The reason genes get "deactivated" is if there is a mutation to some of the surrounding DNA that keeps them from being expressed, or a mutation to their nucleotide sequence that means the protein they code for doesn't work. If a duplicated gene gets duplicated into a part of the genome where it will be expressed, and if its nucleotide sequence isn't altered in a way that makes the protein non-functional, it will be as "active" as the original gene was. (epistatic interactions put a wrinkle on that but I think the principle is there)
Second, genes don't code for feet, or heart speed, or body size, or heart muscles, or veins. They code for proteins. When a gene is duplicated and continues to be expressed it can have results such as twice the normal amount of proteins being produced, or more or less than twice depending on the interactions with other genes, or those proteins being produced in a different part of the body, or at a different point during development, so on so forth. Such differences in proteins can be harmful, but they can also be beneficial. More often they're neutral.
There are genes that can be said to "code for" macroscopic structures like limbs or organs, but those are the regulatory genes you're ignoring. And even there duplicating them won't always have the same dramatic consequences - it really depends on the gene and where they got duplicated to.

I believe the balance of evidence at the moment is pointing to the sudden appearance of already advanced life-forms. (the evidence being the difficulty to create new good active genes).

Up to now I thought you were saying it was impossible for nature to create new active genes, is this a change in position, a different way of saying the same thing, or did I misinterpret your original position ? If I did I apologize. I would still like to know how difficult you think it is to create new genes. Like, in a population of 1000 individuals how many generations would you expect to pass before you saw a single new gene ?

Thus no new genes are needed, You seem to think that evolving should occur anyway. Its absolutely unnecessary if the design was good in the first place. Yes the number of allele combinations is multiple trillions times by multiple trillions so the ability for each creature to adapt to its environment is already there, but you do not need more than that with well designed creatures.

I'm not talking about "need" here. I'm talking about what statistics say will happen given what we know of how mutations work. Now you do bring up another valid barrier to new genes arising : if every organism were so perfectly adapted to their environment already that absolutely no mutation could be beneficial then beneficial new genes couldn't arise. But given we've already agreed that beneficial mutations can happen I'm not sure why you bring it up.

Again were those HAR regions designed or created like that ? Its hard to tell when we just know its there already. Yes there's other aspects important to evolution but I still want to focus on the necessary process of adding extra good protein-coding genes so I do feel that's a distraction.

Well of course those HAR regions, like every single other thing in the Universe, could have been "designed and created like that" by an omnipotent creator. So could any gene that looks as if it's a result of duplication and mutation, so I'm not sure why it's a distraction. I have no issue with people who think God created life and made it look as if it had evolved; it's not scientifically testable but people's personal beliefs don't have to be scientifically testable if they don't want them to be. That said it's true I keep forgetting that you draw a sharp distinction between new genes formed from existing genetic material, and new genetic material, and HAR are an example of the former. Sorry about that.

I deleted one post when I realised I was replying to your same post twice, maybe that's it. If you describe what I said we could talk about it, but I think we have enough to go on, and I like to keep narrowing the conversation to a conclusion rather than increasing discussion topics, which can get impossible to deal with.

Yes that was it; I remember being rather confused by the response so I'm glad you ended up editing it ^^

EDIT : Because it seems you edited your post after I started this response, so I'll respond to the added bits here :

2) They both have the same disabler (indels) which definitely points to subsequent non-coding, they wouldn't call the disabler an indel if it was already there.
3) They could both have independently gained non-coding regions in the same place because of the same environmental pressures on both types of apes as can be seen in the human Duffy gene.

2) As I said, mutation is a completely reversible process. Whether a mutation is "disabling" or "enabling" is really an assumption of which version of the gene came first. I agree it's confusing that they'd refer to "disabling" mutations in the primate genomes; I figure it must be their habit to refer to non-functional bits of DNA in reference to the functional genes they resemble regardless of which came first. It is crystal clear however that they think the non-coding primate DNA bits came first; one can disagree with their conclusion but you can't really use their confusing language to suggest they don't really think what they wrote a whole paper to say...
3) The issue isn't that the regions are non-coding, it's that they're non-coding in the exact same way. Functional, coding regions we might expect to be similar because they're constrained by their function. Not so with non-coding regions. When disabling a gene is selected for (as you say is the case with the Duffy gene), then any mutation that disables it works. There is no reason to expect it to be disabled the exact same way in four different populations.

Down's syndrome produces extra proteins, i assumed because the duplicates are active. Either way, I suppose the syndrome points to additional activity to the norm being destructive. I feel this is generally observable.

(this is probably a bit I missed more than that you added, but anyway) : additional activity to the norm can be destructive, especially when the difference is as huge as what you get with Down's syndrome, but it isn't always. And I am still confused by your terminology : if having a duplicate that's expressed counts as a new gene, then again we've got tons of non-harmful cases of that if only in plants.

#74 joman

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Posted 13 June 2012 - 10:05 AM

.....researchers trying to compare the human and chimpanzee genomes found that a lot of genes that make muscles in the chimpanzees are inactivated in humans, especially around the face.


The researchers suggested this could have.....

.

We also know that subtle changes in regulatory genes that make the same genes activate in different places or at different times can lead to big differences.

Therefore, similarities and differences between creatures denoted at the dna level are not proven to be related to genealogies.

It seems that unscientific bias is used to interpret differences and similarities

It is now apparant that dna is put to use in various ways by unknown means, according to an unknown plan, and according to an unknown methodology.

Therefore, many things being suggested concerning dna are not objective scientifically, but are instead based on personal belief 's concerning the theories of macro-evolutionary change.

#75 aelyn

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Posted 13 June 2012 - 10:47 AM

Therefore, similarities and differences between creatures denoted at the dna level are not proven to be related to genealogies.

It seems that unscientific bias is used to interpret differences and similarities

It is now apparant that dna is put to use in various ways by unknown means, according to an unknown plan, and according to an unknown methodology.

Why would you say such a thing ? Geneticists know quite a lot about how DNA works and how it relates to phenotype. They also know how much they don't know, and have concrete plans on finding those things out. It's probably the most active field in biology today and scientists' understanding of the processes at work is improving all the time. Not knowing everything about a process is a far cry from that process happening by "unknown means" according to an "unknown plan" and an "unknown methodology".

Therefore, many things being suggested concerning dna are not objective scientifically, but are instead based on personal belief 's concerning the theories of macro-evolutionary change.

Have you even read the abstract of any of those papers that suggest things concerning DNA ? Have you kept up to date on the current scientific understanding of genetics, the methods that are used and why ? Your very vague statements show no sign that you did, and as long as that's the case I don't see what there is to discuss. Come with a specific objection to a specific argument made in a paper that's suggesting something about DNA you disagree with and we can talk.

#76 joman

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Posted 13 June 2012 - 12:52 PM

....or they may have a damaging mutation that has an unexpected benefit in a new environment.

I know of no experimental evidence of this. (and you use of the word "may" implies this)
Proof of adaptation or creation of a new trait by means of chance mutation requires experimental proof that the adaptation or trait in question will not predictably arise in isolated populations of the same kind, under the same stresses and conditions.

Thus you get a new subspecies with unique abilities that your average member of the previous population never had.

Proof of never having the adaptation or trait is required..
New can only be proven or not proven, by experiments that show that no other members of a population can be expected to obtain the adaptation, or trait, or that, other isolated populations are found having the adaptation or trait.

I predict that it will never be proven that any population adapts to changes accidentally but, always in direct response to stresses and conditions demanding or encouraging the adaptation.

If chance is involved then changes will not be predictable, nor arise in a timely manner.

The potential for uniqueness is infinite, because the number of different allele combinations is infinite within each population, so personally I do not have a problem with certain "evolving".

An infinity of possibilities is the very thing that proves the impossibility of any new thing arising. As Solomon noted, "there is nothing new under the sun."

For example, consider 1o,ooo coincidences occurring within a set of infinite possibilies.

Thus, thinking it rational to suppose that evolutionary change can ever lead to any macro-evolutionary change is philosophical and not factually based on objective scientific proofs.

Variation within a particular kind is, not related to the topic of macro-evolutionary theory because, what forbids macro-evolutionary change is the law that "kind begets kind", which law allows "variation within kind".

A law of nature excludes possibilities of anything occurring contrary to said law.
Falsification of a stated law merely requires one indisputable example to the contrary of the law.

There are always found to be reproductive limits confining each kind of creature within its kind.

....there may not be pure stasis because of mutations occasionally causing devolving into more fit yet reduced genomes (Duffy gene) , or changing the emphasis of a gene (nylon eater), but you do not observe "added active beneficial genes"

The nylon eater is actually an enivornmental biological garbage desposer. Its ability to eat nylon as been proven to always be expressed when the need arises. (alternative food shortage and available nylon)
This will be found true of all chance related adaptations occuring within a kind.
.

Thus to spend too much time arguing against all possiblities of natural selection is illogical, natural selection does occur, organisms can evolve certain abilities through changes to alelle frequencies and changed or "dead genes", but higher life forms cannot evolve because no natural process actually creates unique functional genes.

Natural selection is an "after the fact", GO/NO GO or, PASS/FAIL result.
Therefore, it is not related to the subject of "how" any change occurred.

The statement, "organisms can evolve abilities through changes to alelle frequencies" is meaningless because, (if by "evolve" we mean "create a function") there exists no actual possibility of it due to the improbability of purposeless coincidental changes combining to present a new function while meeting all the requirements of fit, form and function as necessary to system design goals.

Again, it seems that many fail to comprehend grasp the measure of the improbabilities being multiplied by each needed change necessary to create a purposeful function.

#77 joman

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Posted 13 June 2012 - 01:05 PM

Why would you say such a thing ?

Because you admitted in your post that the conclusions being suggested were based on bias towards evolution as you are presenting it.


Geneticists know quite a lot about how DNA works and how it relates to phenotype. They also know how much they don't know, and have concrete plans on finding those things out. It's probably the most active field in biology today and scientists' understanding of the processes at work is improving all the time. Not knowing everything about a process is a far cry from that process happening by "unknown means" according to an "unknown plan" and an "unknown methodology".

I never implied or said any of this about any geneticists.
What I pointed out is that the biased interpreters of various studies are doing is jumping to conclusions favoring their theories. And, your posts evidence that they are doing so to such a degree as to be to a large degree unconcious of doing so to a fault.



Have you even read the abstract of any of those papers that suggest things concerning DNA ?

If you have the least proof of evolutionary change based on chance and leading to the creation of an adaptability or a trait, present it. Reading abstracts with suggestions for conclusions being made by biased researchers is not amenable to clarity of debate on this topic.
Present your data and will discuss in front of all readers rather than me try to explain to you the holes in the statments of the researchers or the lack of conclusion offered by their research.

Have you kept up to date on the current scientific understanding of genetics, the methods that are used and why ?

To be honest, I don't have to. You are free to find use any excuse you wish to avoid me, but, I ain't hiding am I? You be the expert and present any clear case evidence concluding evolution of adaptations and traits by mutation or chance of any kind.Then will see if you have any case at all.

Your very vague statements show no sign that you did, and as long as that's the case I don't see what there is to discuss.

There is nothing vague about anything I say.

Come with a specific objection to a specific argument made in a paper that's suggesting something about DNA you disagree with and we can talk.

Its not on me to do so. I already know you can't present any evolutionary change as I have defined it. All data fits design by a intelligent purposeful creator.

#78 NewPath

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Posted 14 June 2012 - 02:48 AM

When you say "both apes", are you referring to the non-human apes whose genomes were looked at in the study ? If so you should have looked at it before responding. Quoting from the abstract : "Furthermore, chimp, gorilla, gibbon, and macaque share the same disabling sequence difference, supporting the inference that the ancestral sequence was noncoding over the alternative possibility of parallel gene inactivation in multiple primate lineages."
Please don't tell me you're saying it's possible that chimps, gorillas, gibbons and macaques are sub-species of one another :)
(If you are saying that I'd have to ask what definition of "sub-species" you're using, and why humans don't belong to that species too)


You have to look at the chromosomal patterns to see if they are sub-species or not. I'm trying to define creationist thinking with commonly used evolutionist scientific terms, the attempt may not work though :) My view: A species is an organism created with a unique chromosomal pattern. A sub-species is an organism with changes to that specific pattern that are commonly observed eg indels, non-coding regions, extreme changes to allele frequencies, duplications, ERV's , these changes rendering a changed look and behaviour. If you have unique active beneficial genes in each organism with no signs that they both had these same coding regions, this would show differing species, not a sub-species.

I've looked at the human/ape genome sequences and there are far too many unexplained differences to pronounce them being the same original species. These differences can be explained only by unobserved processes (new unique beneficial genes) or by creation. I haven't yet looked at the 4 apes' genome sequences, if their chromosomal patterns are really closely matching with a few differences occurring through the commonly observed processes, then they could have had a recent "common ancestor" just like dogs have a recent common ancestor with wolves as claimed by most creationists, I have to look at their chromosomal patterns to decide whether they are sub-species or created differently.

You refer to "several mutations in 4 different lineages". I thought we are talking about ONE mutation in four different lineages, a mutation of a non-coding region in these four apes genomes. I already explained that the explanation given by scientists for this is INDELS, which are SUBSEQUENT insertions and deletions, which caused the disabling. Thus this was a previously coding region that became disabled according to the scientists own usage of the terms "disabler" and "indel". Its not just the term "disabler" which creates this impression, they specifically mention "indels".They appear to be contradicting themselves by using those terms, and using evolutionary assumptions to reach their conclusions. If under evolutionary assumptions, a scientist says "this creature evolved from that creature" and you are subsequently using that as support for evolution is circular reasoning. We have both looked at the evidence itself which is 4 apes showing a non-coding region via indels, and humans have that same region yet protein-coding. This is not conclusively a gene adding process, therefore you have no point if you are looking at the evidence itself and not the evolutionist's assumptions of their own evidence.

Additionally , whenever there is a viral attack on all similar creatures, all populations would benefit from the same region being disabled. You say unlikely, I say definitely observed and recently occurring (in human populations after the dispersion).
A silent allele in the Duffy gene has evolved at least 3 times, its also sometimes found among whites: Wikipedia: Duffy Gene
The silent allele has evolved at least twice in the black population of Africa and evidence for selection for this allele has been found.[7] The selection pressure involved here appears to be more complex than many text books might suggest.[8] An independent evolution of this phenotype occurred in Papua New Guinea has also been documented.


Of course I acknowledge this possibility, as you point out I acknowledged it in my response to you, and not only in the bolded portions either (that paragraph about mutations being reversible and us not being able to tell which way they'd gone just from looking at two genes ? That was a direct statement that it could have been a de-activation).
Can we agree that the authors of the paper also acknowledged this possibility and made substantive arguments for why they dismissed it ?

Who really cares what the authors say, its important for us to divorce ourselves from their conclusions and look at the evidence itself. Which is 4 apes having a non-coding region that the scientists say is caused by indels, and humans having protein coding in that region. That is all the evidence presented, and that evidence can certainly be interpreted differently to the scientists' conclusions. The true conclusion here is that this example is evidence that scientists can easily misinterpret their own evidence due to their evolutionary assumptions. Honestly. I hope you are starting to see a pattern here, that is ever-frustrating to creationists.


Is it interesting speculation that Pluto orbits the Sun ? Such an orbit has never been observed. For that matter, until last year such an orbit of Neptune had never been observed either. The creation of a new gene hasn't been observed from beginning to end, but "hasn't been observed" and "appears impossible" are two completely different things. Given everything we've agreed upon about how genes work, the creation of new active genes doesn't only appear possible, it appears to be inevitable. I understand you disagree with this but I'd like to have an argument as to why this isn't true. "We haven't observed it therefore it's impossible" doesn't work.

New active BENEFICIAL genes? Naaa, new genes are created, we have both acknowledged that, but they are neutral or damaging.

I'm also a bit confused by your use of "activate". Maybe you mean "being expressed" ? But we do know of duplicate genes being expressed, the papers we've been discussing are full of examples. And whether a gene is expressed or not depends purely on its nucleotide sequence and the nucleotide sequence of the DNA around it, so changing a gene's expression and changing the nucleotide sequence of a stretch of DNA is the same thing.

Yes, I mean expressed through active protein coding. Introducing new protein coding genes occurs in nature, but is neutral or damaging.



Now you are absolutely right that damaging mutations are much more common than beneficial ones, so that when we look at two almost-identical genes, one functional and the other one not, the most likely scenario is that the non-functional one comes from the functional one. One can't just assume that the functional one came from the non-functional one and is an example of a new gene. But two things : first, this is not what the geneticists who claim to find new genes do. They have actual arguments why they think they've found a new gene, and you should address those instead of mischaracterizing their position as "claiming proof of evolution" just because they "came across a section of the genome that is identical in two species yet the one is activated and the other de-activated".

I understand what you mean here, its just that unfortunately you are using their studies to make that claim. Their studies will be 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.

And second, while it is true it is less likely for a mutation to turn a noncoding stretch of DNA into a gene rather than the opposite, your argument is much stronger than that : you are saying it's impossible. That argument is what I would like you to justify.


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.

Neutralists hypotheses emphasize the importance of mutation, purifying selection and random genetic drift.[3] The introduction of the neutral theory by Kimura,[4] quickly followed by King andJukes' own findings,[5] led to a fierce debate about the relevance of neodarwinism at the molecular level. The Neutral theory of molecular evolution states that most mutations are deleterious and quickly removed by natural selection, but of the remaining ones, the vast majority are neutral with respect to fitness while the amount of advantageous mutations is vanishingly small. The fate of neutral mutations are governed by genetic drift, and contribute to both nucleotide polymorphism and fixed differences between species.[6][7][8]

I've just categorised myself, I'm a neutralist.

I believe in advantageous mutations, they are rare, they never involve extra novel coding genes.


I'm sorry but this isn't how genes work at all. For one thing, there is no reason the duplication would be "inactive" to start with. The reason genes get "deactivated" is if there is a mutation to some of the surrounding DNA that keeps them from being expressed, or a mutation to their nucleotide sequence that means the protein they code for doesn't work. If a duplicated gene gets duplicated into a part of the genome where it will be expressed, and if its nucleotide sequence isn't altered in a way that makes the protein non-functional, it will be as "active" as the original gene was. (epistatic interactions put a wrinkle on that but I think the principle is there)
Second, genes don't code for feet, or heart speed, or body size, or heart muscles, or veins. They code for proteins. When a gene is duplicated and continues to be expressed it can have results such as twice the normal amount of proteins being produced, or more or less than twice depending on the interactions with other genes, or those proteins being produced in a different part of the body, or at a different point during development, so on so forth. Such differences in proteins can be harmful, but they can also be beneficial. More often they're neutral.
There are genes that can be said to "code for" macroscopic structures like limbs or organs, but those are the regulatory genes you're ignoring. And even there duplicating them won't always have the same dramatic consequences - it really depends on the gene and where they got duplicated to.


I beg to differ. Genes are where the trait is genetically coded. The DNA is the core structure for the organism, and coding genes are the source of the expression of each trait. Change the allele, you change the organism. Change the allele frequency and you change the expression of a trait across the population. This is where traits come from, genes. The information storage of these traits is through acids and activation of these traits is via protein-coding. 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 fitness of the organism. This isn't just a principle, its OBVIOUS that damage would be caused when you over-express protein-protein interactions, its logical you cannot have one trait overexpressing itself in a balanced organism. (Down's syndrome). Not only is this obvious, it is observed. The principle is observed and supported by reality.

As opposed to the creation of novel beneficial DNA which is not observed and opposes this principle.

Up to now I thought you were saying it was impossible for nature to create new active genes, is this a change in position, a different way of saying the same thing, or did I misinterpret your original position ? If I did I apologize. I would still like to know how difficult you think it is to create new genes. Like, in a population of 1000 individuals how many generations would you expect to pass before you saw a single new gene ?


My original position was that novel protein-coding genes need to be beneficial to the organism. This is where the genetic information that makes up an organism is contained and activated. Thus to create a complex organism like a human, you need more beneficial protein coding genes than bacteria. Creation says they were created, evolution says they were added, new novel extra beneficial genes were created by natural processes.

So I have not changed my position at all, I have always admitted that additional duplicate non-coding genes can have a benefit (hardiness - backup systems), but if you add coding genes (which you can) these remain neutral or are damaging. My views are developing as I learn more about this every day, but my core argument was openly expressed from the beginning. For evolution to be true, a human requires extra beneficial coding (non-viral) genes to evolve from bacteria, this process is not observed in nature.



I'm not talking about "need" here. I'm talking about what statistics say will happen given what we know of how mutations work. Now you do bring up another valid barrier to new genes arising : if every organism were so perfectly adapted to their environment already that absolutely no mutation could be beneficial then beneficial new genes couldn't arise. But given we've already agreed that beneficial mutations can happen I'm not sure why you bring it up.


LOL, the semantics! I am looking for extra beneficial coding genes, these genes are required for a less complex organism (bacteria) to evolve into a more complex organism (human). Beneficial mutations occur, but they involve destroyed genes or adapted genes, not new genes. De-complexity over time, de-volution, evolution is not observed.

Organisms are not perfectly adapted to ever-changing environments, allele frequencies need to change when confronted with a new environment, that is a God-given (let's say intrinsic) part of organisms. Sometimes a deleterious mutation helps too because diseases appear to be increasing in number, so to de-activate a gene would de-activate that trait in situations when disease is attacking that trait, and therefore deletions or disabling of coding regions can actually help. Thus mutations can have a function, but through devolution not evolution. (Neutralist theory)



Well of course those HAR regions, like every single other thing in the Universe, could have been "designed and created like that" by an omnipotent creator. So could any gene that looks as if it's a result of duplication and mutation, so I'm not sure why it's a distraction. I have no issue with people who think God created life and made it look as if it had evolved; it's not scientifically testable but people's personal beliefs don't have to be scientifically testable if they don't want them to be. That said it's true I keep forgetting that you draw a sharp distinction between new genes formed from existing genetic material, and new genetic material, and HAR are an example of the former. Sorry about that.


What new novel genes "look as if they are the result of duplication and mutation" and benefit the organism? I'm saying both processes are not observed.

I'm not saying God created genes to look evolved, I'm saying genes do not look evolved. Which genes do you say "look evolved", I've dealt with the human/ape situation. Only bias makes them look evolved to evolutionists.




additional activity to the norm can be destructive, especially when the difference is as huge as what you get with Down's syndrome, but it isn't always. And I am still confused by your terminology : if having a duplicate that's expressed counts as a new gene, then again we've got tons of non-harmful cases of that if only in plants.


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. When are new extra protein-coding genes beneficial to an organism?

Most duplicates in plants are non-coding, these are normally neutral, and can have some benefit. Can you give example studies of duplicates that are coding and beneficial?

#79 NewPath

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Posted 18 June 2012 - 10:59 PM

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.

#80 NewPath

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Posted 18 June 2012 - 11:59 PM

I know of no experimental evidence of this. (and you use of the word "may" implies this)
Proof of adaptation or creation of a new trait by means of chance mutation requires experimental proof that the adaptation or trait in question will not predictably arise in isolated populations of the same kind, under the same stresses and conditions.

Proof of never having the adaptation or trait is required..
New can only be proven or not proven, by experiments that show that no other members of a population can be expected to obtain the adaptation, or trait, or that, other isolated populations are found having the adaptation or trait.


I don't see your point regarding about "predictably arising". If traits predictably arise in a population, but are de-selected because lack of function this does not show any evolving. If they are selected because the trait has a benefit to the population then this is some sort of evolving. It is a change to the organism through mutation that becomes more fixed in a population than previously. The organism as therefore adapted to the new environment. The famous "Duffy gene" is one such example. Genes are regularly disabled through mutation, this is predictable, disabling the Duffy gene causes resistance to Malaria, and therefore independent populations can develop the widespread prevalence of the same disabled gene in Malaria infected areas. This shows that organisms can be naturally selected to adapt to their environment through regular predictable mutational processes.


I predict that it will never be proven that any population adapts to changes accidentally but, always in direct response to stresses and conditions demanding or encouraging the adaptation.

If chance is involved then changes will not be predictable, nor arise in a timely manner.

True! There is no need to adapt if the environment does not change.


An infinity of possibilities is the very thing that proves the impossibility of any new thing arising. As Solomon noted, "there is nothing new under the sun."

For example, consider 1o,ooo coincidences occurring within a set of infinite possibilies.

Thus, thinking it rational to suppose that evolutionary change can ever lead to any macro-evolutionary change is philosophical and not factually based on objective scientific proofs.


I disagree with your point here. There have been experiments where they kept breeding flies for the new trait of faster reproduction. They found that various populations developed differing allele combinations for the trait, over many generations. So two populations can have the same trait, yet get there in different ways. This just opens our eyes to the wide potential of an organism to get keep emphasizing a trait, to maintain that trait you need an environment that changes, and gradual enough change over many generations for the entire organism to settle into new allele combinations that can support that trait. As with breeding dogs or any other attempts to rush this process, you will end up with problems, but changed allele frequencies can be beneficial.


Variation within a particular kind is, not related to the topic of macro-evolutionary theory because, what forbids macro-evolutionary change is the law that "kind begets kind", which law allows "variation within kind".

A law of nature excludes possibilities of anything occurring contrary to said law.
Falsification of a stated law merely requires one indisputable example to the contrary of the law.

There are always found to be reproductive limits confining each kind of creature within its kind.


I am prepared to agree to disagree on this. What I observe is that a small dog-like predator in Australasia, Madagascar and South America all look the same. Yet these are isolated populations since the flood. Unless Noah deliberately went around the world placing marsupials in Australia that fill every environmental gap there, and civets and Lemurs in Madagascar? I believe these creatures rapidly adapt to fill ecological gaps, only further genome sequencing can determine whether I'm right or you are right.

The nylon eater is actually an enivornmental biological garbage desposer. Its ability to eat nylon as been proven to always be expressed when the need arises. (alternative food shortage and available nylon)
This will be found true of all chance related adaptations occuring within a kind.]

Natural selection is an "after the fact", GO/NO GO or, PASS/FAIL result.
Therefore, it is not related to the subject of "how" any change occurred.


I don't understand your point here, after the fact means that new populations can appear after a bottleneck when a certain trait "passes" and others die off in a new environment. You end up with MORE of the new trait around, and due to the higher populations and concentrations of that trait, further pressures and bottlenecks can highlight the trait even more. Its not impossible for some members of this new population to have a unique allele combination that is even more beneficial for that trait.

The statement, "organisms can evolve abilities through changes to alelle frequencies" is meaningless because, (if by "evolve" we mean "create a function") there exists no actual possibility of it due to the improbability of purposeless coincidental changes combining to present a new function while meeting all the requirements of fit, form and function as necessary to system design goals.


Its possible that a starving kangaroo will bend down and start chewing a dead carcass when there's no food left because of over-populations of herbivores. The one with the best stomach acids to handle meat will survive. The strong survivors band together and after a few generations you have a well-adapted carnivore. Simple- new environment - new function, and soon, new look. Yes this ability was always latent, as are the variety of leg lengths and strength of jaw etc. After all there are billions of base-pairs for differing allele frequencies.




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