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Author Topic:   How do "novel" features evolve?
Wounded King
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Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


(2)
Message 26 of 314 (655979)
03-15-2012 7:04 AM
Reply to: Message 21 by Chuck77
03-15-2012 6:00 AM


I'm not like Tangle, I'm happy to stick my oar in uninvited.
A clade is a different type of division than species, family or genus. A clade refers to a particular species and all of its descendants. So a clade could be at any level of the Kingdom to Family spectrum provided all the members shared a common ancestral species. The more equivalent term would be taxon since that can also refer to groupings at many different levels. The difference between clades and taxons is that taxon is a more flexible term and can accommodate groupings on bases other than the common phylogenetic ones.
So in the case of the Felidae they represent a clade because they "have all descended from the same ancestor." Every single one of the levels in that scientific classification you posted from Wikipedia might represent a clade.
so to address the specific question ...
Is Felidae a clade or a family?
The answer is that it is both.
TTFN,
WK
P.S. I see that you have resolved this yourself, but I'll post it anyway since I went to the bother of typing it out.

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Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


Message 34 of 314 (656571)
03-20-2012 8:10 AM
Reply to: Message 32 by Chuck77
03-20-2012 1:43 AM


Re: Semantics
The biological species concept defines species based on their capacity for interbreeding and producing viable offspring, usually in the wild. So under the BSC a donkey and a horse would constitute different species since although they can interbreed the offspring, mules, are sterile.
If this was used as a basis for kinds then there would be several hundred thousand, if not millions, of them to be accommodated on the Ark. Most of those would be insects but there would still be tens of thousands of vertebrates to accommodate even if we left all of the fish species out of the picture.
TTFN,
WK

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Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


(1)
Message 43 of 314 (659743)
04-18-2012 11:53 AM
Reply to: Message 42 by RAZD
04-18-2012 9:09 AM


Re: how populations evolve
Do you agree that ... does not exist in either the ancestral species (Wolf) or in other dog breeds?
If he does he would be wrong, there are several other breeds of dog that have webbed paws. Most of these are dogs bred as retrievers particularly for hunting water fowl. Newfoundlands are far from unique in this respect.
TTFN,
WK

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Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


(1)
Message 59 of 314 (659837)
04-19-2012 6:10 AM
Reply to: Message 55 by frako
04-19-2012 4:44 AM


Dog breeds are not the product of natural selection.
See, this is the danger of just so stories. While your narrative is very neat and all it bears no relation to reality. These sort of dog breeds didn't evolve in wild packs on islands through natural selection. They evolved by artificial selection on domesticated dogs through controlled breeding in line with what traits humans considered to be valuable, regardless of whether they were traits that would constitute fitness in a natural environment.
Intellen has already demonstrated a stunningly flawed grasp of evolution. He doesn't need us to tell him even more things that are wrong.
TTFN,
WK

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Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


(1)
Message 73 of 314 (659883)
04-19-2012 12:38 PM
Reply to: Message 71 by intellen
04-19-2012 12:34 PM


Re: how populations evolve - when is it "novel"?
No you are wrong. The basis of the changes in the hereditary traits is not natural selection but mutation, recombination and other factors which alter the genetic material or related heritable information.
Evolution is the result of the operation of selection on the heritable variation generated by these processes.
It is surprising how many creationists/IDists seem unable to grasp this distinction.
TTFN,
WK

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Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


Message 223 of 314 (661573)
05-08-2012 5:01 AM
Reply to: Message 222 by zaius137
05-08-2012 3:14 AM


Re: creating "information" is either easy or irrelevant
Hi Zaius,
RAZD is by no means saying that there aren't usable metrics for measuring information in the Genome, what he is saying is that creationists/IDists don't use these metrics but instead prefer their own peculiar variations which are rarely if ever actually usable. In the few examples where a metric can be applied, such as Spetner's metrics or Durston et al.'s functional information, to get a value there is little way to relate it meaningfully to any actual biological function or system in order to look at changes in that system.
It seems pretty strange to show us a paper on how evolutionary biologists measure information in a genetic system rather than a creationist one since that was what was asked for.
Why not provide a specific creationist/IDist definition so we can see how it holds up?
When calculating the probability of forming DNA segments from a string of Deoxynucleotides it becomes apparent that problems explaining the persistence of new information is problematical (pointed out by most Creationists).
Well certainly as claimed by most creationists, but is it a relevant claim? You seem to be resorting to the old tried and tested tornado in a junkyard approach which has little if anything to do with evolution. Mutations in DNA don't come about by the spontaneous assembling of a random string of nucleotides. At best you might try to make an argument against abiogenesis with this sort of approach, but it would be a weak one with a host of assumptions needed to prop it up. Calculating the probability of any particular specific sequence of nucleotides or amino acids is essentially meaningless unless you put it in the context of the whole array of possible strings and their equivalent biological functionality.
Even in the case of a completely de novo origination of a novel gene, which is what the paper you cited most closely resembles starting from 0 information, I'm not sure how relevant your approach would be since it seems to ignore the array of equally functional divergent strings.
Now tell me why you think that the information in a genome is not well defined by creationists like Myers when it is clearly in his arguments?
I'm not entirely clear who you are talking about here, do you mean Stephen Meyer? If so then I'd ask what that clear definition is because all the ones I have seen are pretty much a mess and he seems to dismiss commonly used ones like Shannon entropy or Kolmogorov complexity.
TTFN,
WK

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Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


Message 225 of 314 (661602)
05-08-2012 3:04 PM
Reply to: Message 224 by zaius137
05-08-2012 1:31 PM


Re: creating "information" is either easy or irrelevant
Hi Zaius,
I'm not sure if there is a language problem but I am finding your argument rather hard to follow.
I found his statement rather broad in scope
Well how broad? I probably couldn't think of more than a dozen IDist/creationists at most putting forward distinct definitions of information. I would suggest that RAZD's criticisms would cover a substantial proportion of them, as would the similar issues I raised.
Off the top of my head there are ...
Lee Spetner, Werner Gitt, William Dembski, Durston/Able/Trevors (I'm putting them together since they published papers on this together), Doug Axe, John Sanford, Royal Truman and maybe Ann Gauger. There may be some overlap amongst them as well, 'Complex Specified Information' is pervasive, I haven't done an exhaustive comparison.
I know I cited a non-creationist paper but it does provide mathematical validity to my assertion.
I don't think it does, you claim 'explaining the persistence of new information is problematical'. In what way does the paper you cited support this? The paper itself concludes that in the artificial system they study new information could arise rapidly contrary to the predictions of creationists/IDists.
Assuredly, the utility of such information is relevant but not to the basic assertion that DNA is an information storage system.
Again, I don't think anyone has an issue with considering DNA a type of information storage system. The issue is rather the source of that information.
Interesting you mentioned Kolmogorov complexity in your example can you explain why?
Because it is one of the metrics which Meyer discussed in 'Signature in the Cell', and which he rejected in favour of 'Complex Specified Information', though I'm not sure if he means quite the same thing by this as Dembski.
TTFN,
WK

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Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


(1)
Message 281 of 314 (662519)
05-16-2012 11:13 AM
Reply to: Message 275 by zaius137
05-16-2012 12:52 AM


Mutation rates
I think there are several issues with the numbers you are choosing to plug into the equation.
For a start you seem to be ascribing the 3% value to autosomal pseudogenes on no basis whatever. I don't see a single mention of pseudogenes, autosomal or otherwise, in the article you took it from or indeed any source in that article to let us know where the author got that particular value from.
Autosomal pseudogenes and 'Junk DNA' are not synonyms, you can't simply declare that what applies to one applies to the other. So you don't have a reliable figure for 'new pseudogene divergence' which makes the rest of the exercise rather pointless.
Can you explain why you think it is reasonable to ascribe this 3% figure to autosomal pseudogenes? The whole point of using the pseudogenes was to have a sequence set for which neutrality was a reasonable assumption. Can you assure us that this is similarly the case for the DNA that the 3% divergence was derived from?
It is also worth bearing in mind that Nachman and Crowell's (2000) figure is only based on a small sample of 12 autosomal pseudogenes and only included length mutations up to 4bp while indels can be 100s of bp in length. While the frequency of longer length mutations is lower their effect on divergence can be radical. So if a significant proportion of that 3% divergence comes from longer indels then I'd question how appropriate Nachman and Crowell's figure is or alternatively how reasonable it is to try and estimate any divergence time from a sequence divergence estimate including variably long indels. This is why most divergence estimates rely on single nucleotide substitution rates alone.
In the Conrad paper (2011) they themselves suggest a divergence time of ~7MYA based on their new mutation rate data and that is in the light of more up to date sequence divergence estimates than Nachman and Crowell or your 2009 article. They also give a range of calculated average mutation rates (1.18 10−8 (0.15 10−8 (s.d.)) and you seem to have chosen to recalculate to reach a value below the lower end of that range.
I don't really see how this is much more relevant to the topic. Especially since the calculations are based on what are considered neutral regions of the genome that we wouldn't expect to be where we would find adaptive features, novel or otherwise. Without knowing what the mutation rate for adaptive substitutions is and the divergence based on adapative sites you seem to be addressing another question entirely, namely whether there is enough time between the human-chimp divergence to account for the genetic divergence we see based on current estimates of mutation rates. I don't see where novel features come into it, especially if we accept that novel features including protein coding genes can arise de novo from single step mutations a phenomenon for which there is now considerable evidence in many species including 60 such putative genes in humans (Wu et al., 2011).
TTFN,
WK

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Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


(1)
Message 282 of 314 (662524)
05-16-2012 12:09 PM
Reply to: Message 1 by RAZD
03-08-2012 10:47 PM


The origin of novel genes, a related issue.
While responding to Zauis latest posts I came across an interesting review article that discusses many of the molecular bases for novel genes and their phenotypic impact.
The paper is "Origins, evolution, and phenotypic impact of new genes" by Henrik Kaesmann (2010).
It covers coding and non-coding sequences, complete de novo origination, chimaeric origination, segmental duplication, the action of transposable elements and many more mechanisms. It isn't exactly a 'For beginners guide' but there is a lot of good stuff.
Directly relating to the opening post Kaessmann has this to say on a specific phenoypic effect of a gene duplication ...
Kaessmann, 2010 writes:
Another intriguing recent case of new retrogene formation illustrates the far-reaching and immediate phenotypic consequences a retroduplication event may have. Parker et al. (2009) found that a retrocopy derived from a growth factor gene (fgf4) is solely responsible for the short-legged phenotype characteristic of several common dog breeds. Remarkably, the phenotypic impact of the fgf4 retrogene seems to be a rather direct consequence of the gene dosage change associated with its emergence (i.e., increased FGF4 expression during bone development), given that its coding sequence is identical to that of its parental gene. The analysis of fgf4 in dogs thus strikingly illustrates that gene duplication can immediately lead to phenotypic innovation (in this case a new morphological trait) merely through gene dosage alterations.
TTFN,
WK

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Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


Message 288 of 314 (662653)
05-17-2012 5:49 PM
Reply to: Message 285 by zaius137
05-17-2012 3:01 PM


Re: The origin of novel genes, a related issue.
So how did the duplicated gene sequence occur in the first place given no original gene sequence?
It is a bit hard to parse this question. Do you mean how did the original sequence from which the duplicate arose originate? As it stands the question seems nonsensical since the duplicated gene sequences clearly did have original gene sequences.
As for Haldane's dilemma there is a substantial body of literature stretching back decades showing that many exceptions to Haldane's underlying assumptions can be found in actual biological populations, (Grant and Flake, 1974). Population genetics has moved on considerably in the half century or so since Haldane first published on selection costs.
Haldane's 300 generations was based on a very specific model with particular assumptions backing it, to assume it can be used generally as you have is frankly ridiculous.
I found this paper rather thin in explanations. However, I thank you for the citation.
Well it was a review paper, there are plenty of citations if you are keen to dig into the details of a particular mechanism.
TTFN,
WK

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Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


Message 293 of 314 (662676)
05-17-2012 7:47 PM
Reply to: Message 289 by zaius137
05-17-2012 6:06 PM


Re: Mutation rates
My 3% again is form
Yes, its from a web article which provides no reference so we basically have no idea what research the figure comes from or what data it was derived from and certainly no indication that it refers to autosomal pseudogenes, which I think I pointed out quite clearly previously.
Sorry to say this but the junk DNA has been reevaluated upward. Some articles are even suggesting a greater divergence.
Once again you fail to address the actual criticism I made of your position and just double down on insisting your approach is appropriate. If a large proportion of this divergence is due to indel's, and if you read the chimp genome consortium papers (2005) you'll know that it is, then they represent the same issue I already highlighted with regard to the appropriateness of divergence due to length mutations in determining divergence times.
So you disagree with Michael W. Nachman and Susan L. Crowell?
No, I disagree with you. Nachman and Crowell made a specific estimate based on divergences from a specific set of pseudogenes chosen as representing neutral genetic regions and with clear well aligned orthologues. You instead are taking a random number you found on the internet that is no more specific in what it applies to than 'junk DNA' and expecting us to give it equal weight. I point out reasons why this is suspect, especially if that divergence value is substantially based on length mutations, and you just ignore the objections and rely on an appeal to authority despite the authorities in question not making the claims you seem to wish to use them to defend.
Did Nachman and Crowell claim they were looking for a rate to explain novel adaptive mutations? No they didn't.
If you care to actually make some effort and show where I am disagreeing with Nachman and Crowll then please do so.
TTFN,
WK

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Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


(4)
Message 312 of 314 (663081)
05-21-2012 9:54 AM


Too much talking past each other
If the creationists/IDists who have posted on this thread are representative then it seems that there is little if any overlap between what they mean by novel features and what RAZD raised in his OP.
As with the an increase in genetic information a 'novel feature' for a creationist is an abstract thing whose requirements shift as they rule out all the examples for which there is copious evidence. Zaius has just given a few excellent examples here.
A frame shift which produces a novel functional protein from a stretch of DNA with no discernible previous function is dismissed as 'Definitely not new novel functions'. Zaius claims that looking at the evidence supports this but in fact it does no such thing. Ohno characterised the pre-existing sequence from which the nylonase gene was thought to arise as 'very basic ... totally lacking Trp and Asn residues ... not likely to function as an enzyme of any sort'. And yet for this sequence to give rise to an enzyme capable of digesting nylon oligomers does not represent the gain of a novel function according to creationists? I can see that they might make a vague genetic information argument on the basis of the majority of the genetic sequence being present in the right order but to claim that a novel function did not evolve is simply to ignore all the evidence. And to claim this is an examples of 'programmed adaptation' is to make a counter claim for which there is absolutely no evidence.
Claims for 'programmed adaptation' are especially empty since there are multiple experiments in different bacteria where strains lacking nylon metabolising ability have subsequently evolved it through distinct mechanisms (Prijambada et al., 1995; Negoro et al., 2005).
Perhaps if Zaius wishes to discussed the nylon metabolising bacteria in more detail we can take it to an open thread such as 'Is the evidence concerning the Nylon bug being exaggerated'.
As to his comment on the Lenski experiment where oxic Citrate metabolism arose, I am aware of no research which ascribes this mutation to a frame shift. Again it is discounted as not novel enough because anoxic citrate metabolism already existed.
The creationists complain that most of the examples are of duplication and neofunctionalisation seemingly ignoring the fact that these are the mechanisms considered responsible for the vast majority of novel functionality.
They have constructed a crazy argument where any new function based on neofunctionalisation is merely 'adaptation' and any saltational example where a whole novel coding region appears is 'pre-programmed adaptation'. It seems that there is no conceivable evolutionary route to a novel function appearing which they would accept, especially all the ones that we see occurring and have reams of experimental evidence for.
Another common tactic seems to be adding in additional conditions for no good reason, one prime proponent of this method was Bolder-dash who eventually moved to ruling out all evidence from bacterial studies a priori. Zaius seems to be making a similar move by trying to rule out segmental duplications and subsequent mutation as a mechanism responsible for increasing genome size and allowing novel variation and instead insisting we explain it all solely with point mutations.
He also makes an argument complete absent any evidence to support it.
The case of dog diversity is a perfect example of what I am talking about; all dogs have the same sized genome, it has not grown in size even when new traits appear.
Perhaps he can go to the RAZDs previous Dogs will be Dogs will be ??? thread to substantiate that claim, I would suggest that given what we know about copy number variation (CNV) in mammals including humans his assumption that all dog breeds have genomes of identical size is grossly mistaken. Indeed an important role for CNVs in phenotypic and behavioural variation has already been suggested through comparative studies of dog breed genomes (Nicholas et al., 2009).
Looking back at RAZDs OP I'm not sure the real questions there ever got fully addressed. I think there were some problems with his doggy examples, for instance many wolves do exhibit a substantial degree of webbing between their toes so the extent to which this constitutes a novel feature is highly debatable.
To some extent I think the whole approach suffers from ideally requiring us to have a detailed picture of all the phenotypic variation in the ancestral populations of an organism before we can answer it satisfactorily. While we can feasibly do this in short lived laboratory organisms it is far from feasible when looking at extant populations of something like dogs, especially since we can't really rely on the current extant highly reduced wolf populations to give us a reliable estimate of the variation that was in the grey wolf population prior to domestication thousands of years ago and certainly not of the occasional low frequency variants such a population might have supported.
Perhaps another thread is needed as Tangle suggests. One where discussions of entropy and information are firmly ruled out as off topic.
TTFN,
WK

  
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