roohif

The protein on GenBank is: http://www.ncbi.nlm.nih.gov/protein/EDO34687 If you're familiar with how to use GenBank (I'm not!) then hopefully you can get the nucleotide sequence and do your comparison. Can you explain your point of this comparison? As I explained in my last post, I don't see how the anemone and human and the anemone and chimpanzee comparisons will yield anything useful for your position. It is a triviality to say that the best match for the anemone will be the human or it will be the chimpanzee. I don't care which one - they have the same MRCA to the anemone.

Just in case that wasn't easy to follow, here is a more extreme example that should illustrate the point: "I compared a gene from an ant to the corresponding gene in humans, chimpanzees, gorillas and orangutans. In a few cases, the best match for the ant gene was the human!" In contrast to: "I compared a gene from a human to the corresponding gene in chimpanzees, gorillas, orangutans and ants. In a few cases, the best match for the human gene was the ant!"

I decided to have a look into this tonight, and after reading the quote carefully, I'm not sure there is even a claim worth investigating. The way I interpret the above quote is like this: We found 226 genes that are shared between the sea anemone and the human. For each of these genes, we compared the anemone gene to the human gene, we compared the anemone gene to the fruit fly gene, and we compared the anemone gene to the nematode gene. "In a few cases", the comparison of the anemone gene to the human gene was the best match. Does everyone agree that this is what the quote is saying? Now here is why I don't think the claim is worth investigating: The sea anemone is from the Cnidaria phylum The human, fruit fly and nematode are all from the Bilateria phylum Cnidaria and Bilateria are sister clades, and their immediate parent clade is Eumetazoa The MRCA of anemones and humans, anemones and fruit flies, and anemones and nematodes is the same organism. It is trivially true that if you compare a particular anemone gene with the corresponding gene in all available Bilaterian genomes, there will be an organism that is the closest match. "In a few cases", the closest match will be from a human, in other cases from a fruit fly, and in other cases from a nematode. It reminds me of Michael Denton's Cytochrome C table where he observed that a particular bacteria - when compared to a host of eukaryotes - all showed approximately 60%-70%-ish dissimilarity .. what he inferred from those results was incorrect.

Don't fret, I'm still here Just a little engrossed in Bible debates of late. Will get around to the BRCA2 thing "soon".

Okay, let me remove the "I don't recall", and state it a little more plainly: "If introns have some sort of function, it does not change the fact of common ancestry". Same goes for pseudogenes. What would those assumptions be, and how do you think it affected the study? They transplanted the CYC sequence from an animal into a host cell and then changed individual residues to see what effect they had on functionality. If they changed a residue that appeared to be highly conserved across all species, it had a negative impact on functionality. If they changed a residue that was hypervariable across all species, it did not impact functionality. That's about as empirical as you can get ... Just back up a little bit: I'm not talking about proteins that are entirely non-functional here, floating around the cell doing nothing - I'm talking about functional proteins. Not every residue in a protein sequence is important to the function of the protein, and it is in those residues that are neutral that you will find the evidence of common descent. I agree 100% that CYC being conserved does not invalidate a design hypothesis! As I said above, it is in the residues of the sequence that are NOT conserved that both confirms common descent and invalidates separate creation. Creationism cannot explain the pattern of similarities and differences in the parts of the sequence that have no impact on functionality. I have. I have also read your paragraph about the Cambrian shale (multiple times) and I don't really follow. I suspect you are giving a lot of weight to the phrase "vertebrate-like DNA", and as I said in my previous reply, I would need to see the context of their statement to know what that means. As it reads, I think they are just saying "vertebrate-like DNA" means that it has lots of introns. And I don't see how a species having lots of introns invalidates common descent. I think you'll have to be more explicit about your claim before I'll comment. What exactly are you saying?

I don't recall it being a prediction of evolution that introns must not have any purpose; I can understand though why scientists thought they didn't. As for the sequences that have no purpose - I posted some Cytochrome C studies earlier in the thread that replaced particular residues and assessed the impact on functionality. I can't be bothered going back through 170-odd posts trying to find it ... 1. Why is this important? The article is about the eumetazoan gene reportoire. It's not like they said "we found the same complement in genes in sea anemones and humans but we didn't find them in other mammals." Now that would be a noteworthy finding. 2. Genes jump around - I don't see the problem. Again, a notworthy observation would be something like "the locations of genes in the human genome finds a better match in the sea anemone genome than any other mammal". Without a comparison made, there's nothing in that statement that could lead to a contradiction of common descent. 3. Isn't that phrase just a lead in to say that there are lots of introns? Again, lots of introns doesn't immediately point to anything that might contradict common descent. If you think it does, you need to explain how. 4. Again, without a comparison, it's meaningless. If it said something like "80% of the anemone introns are in the same place in humans, but only 20% of the corresponding mouse introns are in the same place as humans", then I might raise an eyebrow or two. Nope - the only parameter I'm setting is that sequences in more closely related animals - like a dog and a human - will be relatively more homologous than the sequences in animals that are more distantly related - like a sea anemone and a human. A figure of 80% is pretty meaningless unless we have something to compare it to. http://www.holysmoke.org/gishlies.htm Yes, there is such a function, but if you want me to comment on something specific, I suggest you try and find that protein again.

I know you never used the word "complex", but "Simultaneous Coordination" sounds suspiciously like "Irreducible Complexity". What is the practical difference between the two? "Creationists tend to skip over a thoughtful procedure of how this would come about, because of their undying faith that God did it." The truth is that neither of us know how it came about, but at least evolutionists devote some time to thinking about it. Learn summin' new every day. Disagree entirely - the homology argument in DNA or protein sequences should work regardless of whether those sequences are under selective pressure or not. The introns are spliced out before the template goes to the ribosome which then makes a protein. The introns are still part of the underlying DNA, and will be inherited in their offspring, and will therefore bear the markers of common descent. Therefore we can use phylogenetic trees. Whether the introns are spliced out makes no difference.

The only philosophical argument we've had was regarding why "Common Design = Common Designer" is not valid. The phylogenetic trees on the other hand are as close as you will ever get to scientific proof of common ancestry. Maybe I'm out on a limb here, but I actually view common descent and creationism as a true dichotomy. Either we are related to other organisms or we are not. What I've always left open - intentionally - is the possibility that God could have created that first organism, whatever it may have looked like. This is not a thread about abiogenesis. Yes I have. Many times. No I don't. Both evolution and design would predict similar DNA across species. What creation does NOT predict are the patterns of similarities and differences in DNA across species - particularly so in sequences that have been shown to be neutral to the function of the organism. And this is where the probability argument comes in. For those parts of the sequence that are neutral, God can choose from a virtually infinite number of possibilities to fill in the gap. There is no reason why one particular sequence could or should be chosen over another. Yet, according to the separate design idea, God just happened to choose them such that the chimp sequence is most similar to the human sequence, the dog sequence is most similar to the seal sequence, and the hippo sequence is most similar to the whale sequence. Why did God do this? Of course you could say that we can never know God's will, but in non-Christian language, that just means "I don't know". On the other hand, common descent explains perfectly why these particular sequences share the patterns of similarities and differences that they do - it's because the mutuations were inherited from their common ancestor. So, in my mind, the choice comes down to accepting common descent, or accepting a God that designed our DNA to look a heck (am I allowed to say the other H-word here? ) of a lot like it evolved, and that's just deceptive. I have no objection to some pseudogenes having a secondary function. What I object to is the absurd idea that the gene was designed in a broken state.

A little from Column A, a little from Column B ... To which I've replied - several times - that design does not, and cannot account for parts of those sequences that have been shown (empirically) to have no purpose. Those sequences can be placed into a phylogenetic tree that matches the consensus tree - which is a prediction of evolution, and not a prediction of design. Do you have the full article? I seem to be missing something - I'm not following your reasoning as to why this would be considered convergent (the excerpt seems to be a handful of non-consecutive paragraphs). The only thing the excerpt makes clear is that there are more introns in anemones and humans than there are in the nematodes and fruit flies, and that by itself doesn't really say a lot. The ultimate test would be to plot the intron sequences themselves onto a phylogenetic tree. There is a list of genomes at http://en.wikipedia.org/wiki/List_of_sequenced_eukaryotic_genomes, if you collect all the data, I'll plot the tree. You can even hide the names of the animals if you like, just like Fred did in the CYC thread. Two other points: 1. You didn't bold the first part of the quote that starts with: "We cannot rule out the possibility, however ...". This is very different to actually claiming that the introns were convergently lost, they are just leaving open the possibility. I can't judge why they made that statement, because I can't see the context. Again, if you can get the full article, I'll have a read. 2. There is a subtle difference between the statement "80% of the genes have clearly identifiable relatives" and your statement "introns in the sea anemone and humans are 80% homologous". "80% homology" means that 80% of the sequence of a single gene matches that of another gene, which is a lot different to saying that 80% of a set of the genes in one organism have a corresponding gene in another organism that looks similar - the degree of similarity of each of those genes is the more important data. And even if one individual gene in a sea anemone was 80% homologous to the corresponding gene in a human, it means nothing until we have something to compare it to. In other words, if the BRCA2 gene between the sea anemone and the human is 80% homologous, then I guarantee you that the same gene in dogs, seals, cows, whales, etc will be more than 80% homologous to the human. That's a testable prediction - go for it

Welcome back! Apart from what I've just read on Wikipedia, no That just sounds like a non sequitur to me. I've never understood how you go from "This is really complex and I don't know how it came about" to "therefore intelligence is responsible". You could use my quote, but then I'd respond with a quote of yours: Does anyone claim that introns are functional? I don't know enough about them, and they would be a long way down the list of things that pique my curiosity. Why would they have mutated away any trace? There will be "common mistakes" because it is the DNA that is copied when a cell reproduces - and that includes the "junk" introns, not the mRNA or protein sequence. The whole idea behind my original post is that point mutations that do not affect the function of the organism in a meaningful way can still reach fixation even though their effect is neutral. If, as you say, they mutate freely, then I would imagine they could be used in precisely the same way that protein sequences can be used to create phylogenetic trees. That is, chimps and humans will appear next to each other on the tree, and so on. If this hypothesis didn't hold, then you might have a point worth exploring.

Hey guys, I'm still around. Real life has been pretty hectic to say the least, will get around to responding when I can!

Natural selection keeps them around because they have negligible selection pressure either way. As far as the cell is concerned, it's just a few more nucleotides to copy. Of course, if there was any intelligence involved in the process, then you could instantly recognise that the gene was broken, and just remove it. So it isn't being "selected randomly", it's neutral. If memory serves correctly, I think many of the genes that were lost in the human lineage were related to our sense of smell. Chimp's sense of smell is much better than humans. Why wasn't GULO deleted? Because gene deletion is random - if the gene has strong selection pressure then natural selection will tend to keep it, otherwise it might just drift out of the gene pool. I'm curious about an implied claim here: that a designer "switched the gene off" - with an element of intentionality (rather than by random mutations). Would you attribute that to part of the fall? Also, did the designer switch it off in chimps and monkeys after the fall?

Sounds like an alignment, not a blast (it's comes up with an error if you try and blast multiple sequences at once). Funnily enough, I see it in conflict with a design model "Common Design = Common Designer", therefore "Different Design = Different Designer"? Why would an omniscient designer use two different solutions to the same problem? I'm thinking that this is where an enormous amount of subjectivity will come into play. On a genotypic assessment, two species might fall under the same holobaramin, but subjective phenotypic criteria might result in the two species being different baramins altogether. With that in mind, we probably should discuss why phenotypic considerations should ever take precedence over genotypic considerations in determining if two species are related. I'd also like to propose a similar challenge to Fred's Cytochrome C thread - posting some molecular sequences without the names of the animals and someone deducing which are the in the same baramins.

I agree, and I apologise. Part of my strategy to not get so frustrated again is to not respond to issues that are outside the scope, or issues that we've gone around in circles on (where my responses haven't been addressed). I'm not going away - I'll still be watching the thread, but will be quite selective in what I reply to (according to the criteria above). If anyone thinks I haven't dealt with a particular point well or at all, then PM me, and I'll respond there. "blasted" or "aligned"? A "blast" takes a single sequence and looks for the closest matches, while an alignment takes several known sequences and tries to line up the amino acids to achieve the highest possible matches. So, if you manually counted the differences (and came up with 39 matches) you may not be doing it optimally, which is what the software is designed for. To double check, are you comparing CYC2_RHORU and CYC_NEUCR? Or others? An alignment on these two definitely gives 40 matches. (Also, even if you get 39 matches, I calculate 64% - 65%?). Neither do I, and there are a multitude of reasons why we might get different results. I do have some criteria for choosing the one that I think is the "official" one. That is, it must be "reviewed", sequenced directly, etc. I note that for the Candida krusei, the data in Uniprot is from the late 60's and early 70's, when the sequencing technology wasn't as advanced - and I think that shows when it says "This is version 87 of the entry ...", so I take that sequence with a grain of salt. I used CYC1_YEAST for Saccharomyces cerevisiae. I probably would say that whatever you found was a different gene, and if we're discussing how similar things are, I think you would have to take the most similar sequence from a particular species. Agree? Yup. And if my memory serves me correctly, I think I read somewhere that he now accepts common descent. So, best be mindful of using any of his arguments against common descent, because if he now accepts common descent you can be assured that he no longer finds those arguments valid, presumably for good reason

I'm still watching the thread, but I'm only going to respond to points that: 1. Are on topic 2. I haven't already addressed So, if you think you have a post that is on topic, and hasn't been addressed before, let me know via PM. Otherwise, don't waste my time. If you think you can get from "I don't know how S@xual reproduction could have evolved" to "therefore evolution is false" you'll probably win a Nobel Prize.