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Author Topic:   Biological classification vs 'Kind'
Wounded King
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Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


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Message 263 of 385 (564689)
06-11-2010 6:36 PM
Reply to: Message 259 by BobTHJ
06-11-2010 5:23 PM


Dr. Borger's articles referenced above give some insight into how to construct a baramin using certain indicator genes like FOXP2 in humans. He doesn't go into this in great detail
No he doesn't, presumably because he just seems to arbitrarily throw up the idea just to let himself state that humans and primates come from different baramins. It doesn't tell us how to identify a baranome or a baramin at all.
This is no less arbitrary than any other creationist line drawing for kinds/baramins. All it means is that they are now drawing these arbitrary lines in genomes rather than morphological taxonomies.
Borger seems to spend all his time miscasting research to his own ends. One example is his example of a baranome for the yeasts. He characterises it so ...
The lack of understanding of baranomes recently led to a severe misinterpretation of the origin of genes in the secular literature. Eager to find evidence for the evolution of novel biological information, a novel de novo protein-coding gene in Saccharomyces cerevisiae was reported on the basis of genome comparison among several species of Saccharomyces. The BSC4 gene had an open reading frame (ORF) encoding a 132-amino-acid-long polypeptide. It was reported that there is no homologous ORF in all the sequenced genomes of other fungal species, including closely related species such as S. paradoxus and S. mikatae. The sequences presented in the figure above demonstrate, however, that the BSC4 gene can be found interrupted and inactivated in S. paradoxus, S. mikatae and S. bayanus.
So the message here is apparently that Borger doesn't understand what an ORF is. The open reading frame is from the ATG right at the start of the sequence in the S. cerevisiae sequence, the other three sequences lack this and therefore have no homologous ORF, they have homologous stretches of DNA, but without that ATG start site they don't have an ORF. So the paper is entirely correct in its statemement. That Borger disagrees with their conclusions and prefers a less parsimonious explanation is far from being enough to substantiate a claim of severe misunderstanding on the paper's authors' part.
Borger's explanation typifies his whole approach, throw out parsimony and make up any explanation no matter how tortuous based on a completely hypothetical baranome of a kind that is frankly impossible to envisage as a functional genome.
This isn't unique to Borger of course, these sort of ad hoc supergenome approaches are common in front-loading forms of ID and creationism. John 'Salty' Davidson, another old habitue of these forums, had a somewhat similar hypothesis, see the thread 'A Prescribed Evolutionary Hypothesis'.
If we throw out parsimony we can come up with all sorts of wacky ad hoc scenarios to explain the evidence, and that is exactly what creationists and IDists routinely do.
TTFN,
WK

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


Message 305 of 385 (565156)
06-15-2010 4:27 AM
Reply to: Message 302 by BobTHJ
06-14-2010 7:05 PM


Interestingly - the insistence upon vestigial organs and junk DNA to support darwinian evolution has actually hindered the advancement of science. When entire organs and sections of the genome are written off as evolutionary remnants there ceases to be a concerted attempt to find their function.
Care to give us anything to substantiate this other than just your word? Given that 'Junk DNA' was a term only coined in the 1972 and by 1992 there was already a growing body of research into functional elements in what had been termed 'Junk'.
By the far the bigger barrier to genetic research has been technical limitations. When Ohno coined the term 'Junk DNA' there was basically no sequencing technology whatsoever, the following year it was a big deal when 25 base pairs were sequenced. Nowadays centres like the Sanger sequence entire human genomes in a day.
So where exactly was this hinderance to the advancement of science? in the 20 odd years between Ohno publishing his paper and functional elements in non-coding DNA being widely recognised? It seems to me that our understanding of the functional aspects of all elements of the genome have only been held back by our technical abilities not any theroretical framework of genetic function.
As to vestigial organs, there is already a thread discussing those , 'Vestigial Organs?'. The simple answer though is that what you and other creationists mean by 'vestigial' is not what Darwin and other biologists mean by 'vestigial', it doesn't simply mean functionless.
TTFN,
WK

This message is a reply to:
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Wounded King
Member
Posts: 4149
From: Cincinnati, Ohio, USA
Joined: 04-09-2003


Message 306 of 385 (565172)
06-15-2010 9:55 AM
Reply to: Message 275 by Percy
06-12-2010 5:10 PM


Re: a deeper understanding
What is the evidence that there is any such thing as VIGEs?
Taken simply as a term there are in fact several well characterised Variation Inducing Genetic Elements (VIGEs). The most well studied ones are probably the repetetive transposable elements such as LINE-1 and SINE. Between them LINE-1 and SINE elements make up ~27% of the genome. There are ~100 LINE-1 elements which still have reverse transcriptase activity allowing for their own reintegration when they are expressed, or the integration of certain other elements expressed at the same time.
Such retroinsertions have been shown to have effects on the regulation of gene expression (Han et al., 2004; Lee et al., 2008) and along with other retrotransposon mediated activity are thought to have played a significant role in genome evolution (Xing et al., 2006;oi/10.1371/journal.pgen.0030166]-->Santangelo et al., 2007; Han et al., 2008;Faulkner and Carninci, 2009). These are relatively recent papers on the topic but such research stretches back to Barabara McClintock's initial discovery of transposition in the 40's and 50's (McClintock, 1950).
Borger hasn't just made all these things up off the top of his head. He's just done what so many creationist/ID proponents do, taken the hard evolutionary research done by actual practicing biologists and tacked on his own specious ad hoc bits to try and fit his favoured scenario.
TTFN,
WK

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 Message 275 by Percy, posted 06-12-2010 5:10 PM Percy has replied

Replies to this message:
 Message 324 by Percy, posted 06-16-2010 7:56 AM Wounded King has replied

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


Message 328 of 385 (565359)
06-16-2010 10:49 AM
Reply to: Message 324 by Percy
06-16-2010 7:56 AM


Re: a deeper understanding
Or is VIGE a real term?
VIGE isn't a term used in biology, it is Borger's own coining which covers ...
Borger writes:
endogenous retroviruses, insertion sequences, LINEs, SINEs, micro-satellites, transposons
Borger makes a serious of totally unsupported assertions which distinguish his understanding of VIGE's from mainstream science.
Firstly he postulates that rather than endogenous retroviruses being the result of RNA viruses being incorporated into human germ line cells, instead RNA viruses are the result of the ERV type VIGE becoming independent of its created place within the 'baranome'. Borger says that this solve the 'RNA virus paradox', a paradox no one outside of creationists and IDists has ever noticed apart from in one paper (Holmes, 2003) which also puts forward several solutions to this apparent paradox. So as seems to be habitual Borger simply throws out the current model and replaces it with one of his own which has nothing to support it.
He also decides to totally throw out all we know about variation which occurs independently of his 'VIGE' mediated mechanisms as well as totally ignoring all the multiple examples of 'VIGE' induced varaition which have absolutely no effect or are highly detrimental, all the evidence in fact that shows that the vast majority of activity of these elements is as random with respect to fitness as any other mutational factor.
TTFN,
WK

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


Message 354 of 385 (565490)
06-17-2010 9:53 AM
Reply to: Message 352 by Percy
06-17-2010 8:43 AM


Winzeler paper
Are you sure that's the right reference? Only the abstract is available to non-subscribers of Science, and the abstract says nothing about redundancy.
I suspect that is the right reference, but it doesn't say what Bob would like it to. One big problem is that Bob seems to be conflating the 2 different concepts of redundant and non-essential genes. The paper ( Winzeler et al., 1999 ) (you don't need a subscription, but you do need to register with the Science website) discusses the effect of several hundred gene deletions and notes that most of these genes are non-essential, meaning that when they are deleted these genes do not cause a complete loss of viability. Of these non-essential genes 8.5% had more than one homologue in the genome, what we might consider gene redundancy. Of the essential genes, those whose deletion caused a complete loss of viability, only 1% had any homologues in the genome. So we can see that gene redundancy seems overrepresented in non-essential compared to essential genes, which seems to me to run totally counter to BobTHJ's claims.He seems to be trying to represent the research as if all of the non-essential genes should have duplicates to be in accord with current evolutionary theory.
It is worth noting that of those non-essential genes 40% of the deletants showed defects in growth in competetive assays, so there is an important distinction to be made between a deletion that does nothing and one that simply doesn't kill you straight away, as the essential deletions do. They don't say how many of the genes in that 40% had duplicates. They also couldn't test every functional attribute of the yeasts so there may be other environments in which some of the remaining 60% would show a phenotype.
So I really don't think this paper says what BobTHJ wants it to at all.
TTFN,
WK
Edited by Wounded King, : Revised paper date.

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


Message 370 of 385 (567214)
06-30-2010 4:57 AM
Reply to: Message 368 by BobTHJ
06-29-2010 7:32 PM


What I was referring to is that the study demonstrates 83% of genes to be non-essential to survival, and of those 60% have no noticeable phenotype. Now, given - phenotypes may exist for some which were not found - for the sake of argument let's assume half of those 60% of non-essential genes would have a phenotype that reduces fitness in the wild (far more than is likely). That still leaves approx. 25% of the expressed genes in Yeast that HAVE NO PHENOTYPE and thus grant no additional fitness.
Well if you wan't to just keep making things up that is fine. But in fact there is no basis for your 25% figure. To say that they 'HAVE NO PHENOTYPE' is simply a baseless assumption, and all caps doesn't make it any less so. All you can actually say is that they don't have any phenotype which produces quantitative growth defects in either rich or minimal medium, since that was the only phenotype that was being assayed.
How does natural selection conserve genes that convey no fitness? The explanation was "those genes are the result of gene duplication", but the study shows this to be the case for less than one in ten.
That isn't the explanation at all, and it certainly isn't what we have been discussing. What the differences in gene duplication between the essential and non-essential genes is used to show is that there are a larger number of duplicates in the non-essential set, making genetic redundancy one possible explanation for the non-essential nature of those particular genes. That has always been the position, that gene duplication produces gentic redundancy making that particular genetic pathway element more robust.
This has nothing to do with conveying 'no fitness', and the study would have no basis to make such a claim. Of course the study doesn't claim this, you do.
It has long been regarded as the case that most unicellular organisms have a much wider metabolic flexibility then metazoa, and yeast is no exception. One screen looked at deletions under a combination of various growth conditions including aerobic and anaerobic as well as using a variety of growth media (Gu et al., 2003). This showed that ... 'there is a significantly higher probability of functional compensation for a duplicate gene than for a singleton, a high correlation between the frequency of compensation and the sequence similarity of two duplicates, and a higher probability of a severe fitness effect when the duplicate copy that is more highly expressed is deleted.' Those results seem to fairly conclusively argue for a role for duplicated genes in genetic redundancy.
TTFN,
WK

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