Evolving New Information

I'd still say you were wrong. Greyseal first brought up the melanic moth as an example of natural selection in Message 163 to which LucyTheApe, a creationist, replied ... RAZD then corrected some of Greyeal's misapprehensions concerning Kettlewell's research, for which Greyseal thanked him. RAZD also thinks the melanic moth is a good example of natural selection. Where is the 'controversial' debate between evolutionists around this topic on this thread/site?TTFN,WK

I wasn't using that as an analogy to genetic mutation, I was just countering Cavediver's contention that a single 'point mutation' in a sentence would render it meaningless. I'm not sure what you mean? Are you saying that viruses can only propagate because animal cells share an almost universal machinery of transcription and translation? As Cavediver said, a cell will just produce the protein that is encoded, if there are mutations in the genetic sequence it will carry out the synthesis according to that sequence. The functionality of the resulting protein will depend upon the precise mutation. I think you mean mutations in DNA since rna is highly transient and a mistranscription from DNA to RNA is unlikely to have a long term effect, certainly not outwith the cell in which it occurs. I also think you are thinking of errors in translation since they could be translated in different ways depending on reading frame, but not really transcribed in different ways.If you were talking about mutations outwith coding regions affecting transcription levels due to regulatory effects that is an interesting question, but from what you say I don't think that is what you mean. Well changes in the 1st and 2nd position within a codon are more likely to result in non-synonymous mutations certainly. Whether this makes them mutations with larger effects depends largely on the specific mutation. Some substitutions will have absoloutely no functional effect on a protein, because they do not change the proreins overall structural form and physicochemistry. We can make some predictions on changes to structure and function in terms of well chracterised functional sequences, but in general the best way to find out what effect a mutation has is to study it in action.As an aside the 3rd base redundancy does mean that we can theoretically change at least 30% of any coding sequence without expecting any functional changes in the protein. Although as Percy highlighted, there is research suggesting it could affect the rate at which the protein was produced.There is plenty of non ID based research into the genetic code and transfer RNAs, which are where any pattern recognition involved is surely occurring. I'm not sure where your ID answer becomes neccessary, there is a well developed understanding of the processes involved and several plausible theories for the evolution of the genetic code.TTFN,WKEdited by Wounded King, : No reason given.

You were doing well up until here. There are a number of forms of mutation which could in fact stop a protein being created. The most obvious is a mutation which removes the start codon for the gene.TTFN,WKEdited by Wounded King, : No reason given.

I don't think you understand what the term 'point mutation' means. A point mutation is when 1 single nucleotide is changed to another nucleotide. It is one of the smallest possible forms of mutation.Klinefelter's syndrome is caused by having an additional X chromosome, changes in chromosome number are one of the largest possible forms of mutation.I am also unaware of any research showing a specific point mutation to be responsible for melanic forms of Biston betularia, as far as I am aware the exact genetic basis is still unclear.TTFN,WK

But you then described it as ... Slightly contradictory. If you want some examples where the genetic basis is known then you could do worse than to look at Kingsley et al. (2009). They discuss multiple genetic bases for melanic forms in a variety of organisms as well as linking to several wider reviews of the topic.They discuss spontaneous mutations in four genes involved in colouration: the Agouti signaling protein (Agouti), attractin (Atrn), melanocortin-1 receptor (Mc1r), and mahogunin (Mgrn).One interesting point in the paper is that ... So this example in some ways counters the common creationist ploy that even beneficial mutations are the result of a loss of information, in some non-specific platonic sense, since it is the gain of function mutation that is most common found in nature.It is worth bearing in mind that a gain-of-function mutation doesn't necessarily really map to a creationist gain-of-information but then what does in the field of genetics?TTFN,WK

This is the sort of claim that really requires substantial evidence. Didn't we just cover the fact that ~30% of a coding DNA sequence could be changed without even changing a single amino acid in the primary sequence of its protein product? That seem like a pretty big margin of error right there. Please show your working. No, you infer it even in the absence of lame explanations. You just infer it from nothing but you own incredulity basically. You could say that, but you would look like an idiot to do so. There are vast numbers of people of faith who support modern evolutionary theory and see it as the best explanation of life's history on Earth. You could probably count on the fingers of one hand the people who aren't religiously motivated who want Intelligent Design taught in schools or put on an equal footing with evolution despite its lack of substantiating evidence. Yes, every couple of years someone publishes a theoretical maths/informatics paper that subsequently sinks without trace. Its not what I'd call a really constructive research cycle. It needn't unless one of these causes is ineffable, intangible, indescribable or in some other way inconsistent with our whole understanding of nature.TTFN,WK

It was in Message 221. It is a consequence of the redundancies in the 3rd base of codons. There is, but surely it is obvious to you that this doesn't translate into knowing what the functional effects of most mutation in most proteins are, it would take an inconceivable amount of work just to screen all the possible single nucleotide substitutions for 1 gene. In most cases this type of research is specifically based on using heavy mutational methods, such as ionising radiation, and looking for large scale phenotypic effects. The entire point almost of such experiments is to break genes by giving them damaging mutations. this is not a technique easily adapted to small effect mutations with subtle phenotypes. As I said in Message 221 I think you are thinking of DNA not RNA. In fact experiments have been done where genes from one species have been 'knocked in' to another and they have rescued the mutant phenotype. It isn't about a working model. You said you knew the probabilities of 'the nucleotides landing in specific sequences in an origin of life model are extremely unlikely'. I wanted to know how you had calculated them. I imagine rather from an absence of evidence. But you aren't inferring an absence you are inferring a presence which surely requires stronger support or at least positive evidence? Again, this would be a really good place to pull out all of your supporting evidence, particularly the published practical research papers. Are you thinking of stuff like Jonathan wells 'research' on cancer which you mentioned before, but which you didn't actually know anything about? Unfortunately this makes no sense to me, are you saying evolution should make everyone an atheist if it is true?TTFN,WK

I'll take your word for it, so far this doesn't seem to have been the case. Wouldn't it be a good thing to have a good understanding of something before criticising it and telling us all what is possible or impossible? Oh, a guess. Wow, good argument there. You really showed me how you weren't just making an argument from personal incredulity. Is that your criterion? If so you have totally failed in understanding how science works and what research is. A review article by Stephen Meyer saying how unconvincing he finds evolution and trumpeting theories which have never been published in a peer reviewed article? There is nothing in that paper constituting research supportive of ID, it is a review article. If you think there is solid evidence then you could start a thread and we could discuss it. I thought there already was a thread where I commented on the PBSW paper, but I can't find it now. If it was a productive field of research I would expect what we see from evolution. A continuing and increasing volume of published research using ID principles to drive it. Oh yes, boo hoo. Mainstream science was mean to ID so it is taking its theory and going home. I'd agree with you about his more recent books, and certainly that the ID books belong there.TTFN,WK

No, of course it wasn't. It is a natural consequence of the degenerate nature of the genetic code. If you accept that third base wobble exists then it naturally follows that you can change up to 30% of most protein coding sequences without changing their primary amino acid sequence. How can you not understand this? If you have evidence contradicting the commonly understood mappings between codons and amino acids then that is pretty exciting news, care to tell us what it is? Yes I do know. You also don't seem to understand the language of biology or information theory, and yet this hasn't stopped you from making numerous assertions about all of these things.I'm not sure what you are doing for the rest of your post. If those are quotes then surely they are from one paper rather than several. If they aren't quotes then what was the point in italicising them.It looks like all of your quotes are actually from the Meyer paper. I am hardly won over by the fact that Meyer agrees with you.I have to say though that this ... Is not really born out by Axe's paper. At least not until you reach a substantial number of substitutions. In fact he replaces 1/5th of all the external sites, even an enzyme with 30 amino acid substitutions still has some functionality. It is idiotically obvious that if you just keep on replacing amino acids you will eventually compromise function. Bear in mind that if you can change 20% of amino acids without affecting function, which also isn't what the paper shows but for argument's sake, then that, in addition to our 30% divergence in the DNA without producing any amino acid substitutions, means that you could change more than 50% of the DNA sequence in some cases and maintain some functionality. I think that if you work the maths out properly it might even be higher. I'm sure you do believe it, the same way you apparently uncritically believe everything you read on ID propaganda sites.TTFN,WKEdited by Wounded King, : No reason given.Edited by Wounded King, : No reason given.

There is a 'great debates' forum for one to one debates. If the dogpiling is a bit too much, and I can see how it would be, that is a more evenly paced alternative to consider.TTFN,WK

This is utterly false, you just don't bother to address the refutations. You always have some other bit of ID nonsense to throw up for refutation. But you don't debate them, you just regurgitate an ID talking point and ignore all the criticisms by going on to another one, and you consistently cite Idist popular 'science' books and review articles as if they are equivalent to peer reviewed primary research. This is the stupidity of creationists and IDists. A good theory should stand on its own merits and with its own supporting evidence. If some central pillar of evolutionary theory were to be shown to be incorrect that wouldn't somehow magically constitute evidence of intelligent design. This is the purest 'god of the gaps' argument, anything that can't be explained yet is assumed to be incapable of explanation. It also totally ignores the fact that evolution can be explained with these things, along with lots of other recognised material biological phenomena. Well you can't in the current system since both those sequences lack a start codon. However that isn't a coherent argument against evolution or even against abiogenesis, which is what it seems more relevant to. Or just wishful thinking.TTFN,WK

Um, we could read the paper. Its not as if peer review is the be all and end all of review in science, it isn't the ultimate seal of approval. To be honest it doesn't matter if the paper was reviewed and approved by Dawkins, Jerry Coyne and PZ Myers its still a rubbishy little review paper which does nothing to show positive evidence for ID and equally little to make a compelling argument against modern evolutionary theory.It seems odd to abbrogate our own critical faculties by saying we can't tell if it has a point or not. You might have a stronger point if it was some primary research where fraud might be an issue, but scientific fraud frequently gets past peer review because that isn't really what peer review is designed to weed out. And in any case it is only a review article, all you need to do to fact check it is see if the references Meyer gives support his argument and whether his argument actually makes senese.In my view the whole rigmarole surrounding the peer review and publication of this paper is incidental to how worthless it is as either science or evidence supportive of ID.TTFN,WK

It seems strange to try and challenge us on our claims based on a claim that no one on this site made. Why not ask us to support some of our own claims, apart from the obvious reason that we have done so in multiple instances, almost always to the detriment of your position.I have to agree that tolerance of 80% amino acid substitutions sounds very high. One would have to assume that this might be the very extreme range of functional conservation, or that most of the substitutions were highly conservative in terms of physicochemistry.A bit of sleuthing on my part discovered that the proteins in question are the Treponema pallidum and Agrobacterium tumefaciens forms of the MOTA flagellar motor protein. You can get their protein sequences from ENTREZ here and here. Put them into an alignment program such as ClustalW and you will see that indeed they do differ in ~80% of their amino acid sequence. Whether this actually goes with no change in conformation and function I don't know, but presumably the flagella function in both species. I might investigate further but this seems to substantiate the idea that 80% amino acid substitutions still produce a functionally equivalent protein even if not a functionally identical one. You may have found instances where this is clearly not the case for many proteins but unless you are actually looking at the relevant case it hardly matters. There is information supportive of the claim, it is just hard to track down because unfortunately the link to it in the original commentary on Meyer's paper is now broken due to changes in the website it targeted. No its not true, it is transcribed in to mRNA which is then translated into amino acids, in some cases. we'd rather you followed one line of argument to some sort of conclusion instead of batting around all over the place. And ideally that you backed your claims up with reference to scientific research rather than popular books. James Shapiro is the right sort of direction to be going Shapiro's work is very interesting, but unfortunately for you it doesn't provide evidence for ID.TTFN,WK

Yes, and the quote relays a claim made by Nick Matzke in an article posted to the Panda's Thumb. Now Nick has posted here you so you could say that someone on this site has made that claim, but they didn't make it here and it wasn't being made here again, someone was simply reporting that they had seen the claim made.The claim was to what the rebuttal paper said, not to the accuracy of its statement.Do you agree that there is in fact also evidence to substantiate the claim? I don't quite know what the point of this paragraph is, but I certainly agree that structurally distinct sequences can perform enzymatically similar functions. Are you claiming that the MotA from one of those bacteria is in fact the product of convergent evolution from an entirely unrelated gene rather than simply a member of the same lineage with a high proportion of sequence divergence? It is quite possible for similar but not identical amino acid substituttions to allow similar conformations, so there is no reason why a non-identical 2ary structure can't give rise to a similar functional fold. No, you got the terminology wrong and I corrected you. Transcription and translation are specific and distinct things. Simplification is not the same as being wrong. If you are using them to back up a substantive argument it shouoldn't be a problme, certainly less so than your indirect attempts to do essentially the exact same thing by directing people to google searches.I can quite believe that 50% substitutions can radically change a proteins conformation, even with a lot of conservative changes, but it depends a lot on the protien and the exact changes. One such example, or even several, does not undermine the example from MotA, it just suggests that the MotA situation is quite rare, which I am quite prepared to believe. No it isn't, it is exactly the subject Shapiro's work addresses and the answer is that much of the engineering comes from transposable elements in the DNA and mechanisms which promote genetic re-arrangement as a response to certain environmental cues or in specific cell lineages, i.e. the immune system in mammals. We also know that effective changes can be produce by mechanisms including single nucleotide substitutions and gene duplications.TTFN,WK

Drew, all you are doing is regurgitating the claims of the ID crowd, claims which you simply seem to accept at face value. Then the reason can only be because you haven't looked. I directed you to specific proteins sequences and the tools you could use to analyse them yourself to determine the degree of conservation. Did you do it? If so did you get a different result to me?If you want to make a case that the different MotA proteins are functionally distinct then make the argument. Just saying over and over again taht there is no evidence is the purest bull when I have given you the best evidence you can have short of us getting together in a lab and sequencing the genes ourselves. Environmental factors such as the pH it was working in, the presence of other proteins, the phosphorylation state of certain resides and a number of other physicochemical factors. But all of these things being equal we would still expect the same sequence to produce the same folds.This is irrelevant though since you concede that other sequences can produce functionally similar, if not the same, folds. And Meyers attribution is enough for you? Do you see why we get the impression you are doing nothing more than cutting and pasting points from ID sites? You don't seem to want to do any research into these topics that doesn't consist of looking up the recieved ID wisdom on them.Take the MotA claim as an example, just give lookign at the actual evidence a shot. Nick Matzke says that the MotA sequences from two species have a conserved function despite having an amino acid sequence identity of only ~80%. If we look at the sequences for the MOTA protein in Treponema pallidum and Agrobacterium tumefaciens then we do indeed find that they differ by around 80%. If you don't trust the links I gave you in Message 335 then go to the ENTREZ site and find the sequences for yourself.If you don't disagree about the percentage then you must be disagreeing about the function, so what evidence are you using to conclude that the MOTA protein does not fulfill a similar function in both bacteria? Do you have specific evidence contradicting the quote or just vague ID platitudes about how unlikely it all is and what delicate fragile unique special flowers every protein is?You could show us a dozen proteins which absolutely require 100% conservation at the amino acid level to function at all and none of them would be evidence contradicatory to Nick Matzke's claim, because none of them would be the MotA proteins he is discussing.Do you think he is talking about different proteins or that I just picked a random protein which has homologues with 80% sequence divergence and claimed that was what he was talking about? I can show you the trail I followed to identify which proteins he meant if you like.Why not look at the actual evidence for once rather than a potted digest handed down from the ID movement?I'm also not sure what you think convergent evolution is, none of the things you talk about are convergent evolution in the sense it is generally understood in biology. Are you saying that homologous genes in the developing wing and the gills are the result of convergent evolution at the molecular level? That the same molecular strutures evolved (or were created/intelligently designed if you will) seperately twice for 2 different functions?As usual of course Behe is talking nonsense. The fact that we find teh same genes in the same sort of regulatory pathways in multiple organisms and multiple organs says masses as to how they have evolved, and the differences in the molecular constitution of those genes and their regulation and the relationship between these and the differences in the actual structures produced is the entire basis of Evo-Devo. And Sean Carroll is right, it was very unexpected. People expected to see much greater divergence and diversity at the genetic level and the existence of such fundamental similar genetic building blocks as the HOX genes and numerous signalling pathways was a radical discovery. But the similarity of these pathways, and indeed the patterns of their diversity, are a strong argument for a natural history of life on Earth based on common descent with modification from common ancestral populations. And the nature of that diversity is consistent with mutational mechanisms with which we are already familiar at levels stretching from the single nucleotide to entire genomes.TTFN,WK