Re: [asa] Two Amino Acid Difference in Gene May Explain Human Speech

Rich, the title of your post is "Two amino acid difference in gene may
explain human speech". Now, I don't have access to the whole paper in
question - so maybe they claim what your title does somewhere in them.
However, at least by what I've read here, it seems that what's being made is
a vastly more measured claim - namely that the FOXP2 gene has an important
role in speech and language in humans. Not that two amino acid changes
"explains human speech", or even "may explain human speech" unless that's
qualified to mean "Be part of an explanation which will likely include
vastly more data".

Further, even the boldest ID proponents do not say that science determines
guidance - indeed, Dembski has outright said that there can be (and in his
opinion, is) design in nature that science cannot detect. At most, ID
proponents argue that an inference to design can be a scientific inference
(and I question that myself).

What's more, ID proponents are not "handing Dawkins a weapon" any more than
they "handed Darwin a weapon". Dawkins does not take orders from Behe - he
and others have been in essence arguing that science is capable of detecting
design *since the Origin of Species*. What's more, they've done this with
the response from the academic community largely being one of turning a
blind eye, or even endorsement of this practice. Then ID came along and
decided to play by these rules - rules that, until that point, treated
design as a question science could answer so long as the answer was "there
is no design".

I sometimes get the impression that some people think no one ever abused
science for social, political, or philosophy ends before ID came along. The
sins of ID are shockingly unoriginal in all ways but particular conclusion.

On Thu, Nov 12, 2009 at 1:17 PM, Rich Blinne <rich.blinne@gmail.com> wrote:

> Genetic mutattions in the forkhead box P2 (FOXP2) gene has long been
> associated diseases in speech pathology --
> http://www.ncbi.nlm.nih.gov/pubmed/11586359?dopt=Abstract&holding=npg.
> When this gene is looked at from an evolutionary perspective it's been noted
> that it has been highly conserved in mammals until the common ancestor of
> humans and chimpanzees. There is a two amino acid difference between the
> human and chimp versions of this gene. The transcribed protein of this gene
> controls the regulation of *other* genes. It's a kind of dimmer switch if
> you will.
>
> Which brings us to a paper in today's *Nature*
> http://www.nature.com/nature/journal/v462/n7270/full/nature08549.html. A
> UCLA team headed by Daniel Geschwind found when using both the human and
> chimp versions of the FOXP2 *in vitro* with human brain cells:
>
>
>> We identified 61 genes significantly upregulated and 55 genes
>> downregulated by FOXP2 compared to FOXP2chimp (Supplementary Table 1<http://www.nature.com/nature/journal/v462/n7270/suppinfo/nature08549.html>),
>> as well as genes regulated by both FOXP2 and FOXP2chimp (Supplementary
>> Table 2<http://www.nature.com/nature/journal/v462/n7270/suppinfo/nature08549.html>
>> ).
>>
>
> They then went a step further. They checked the regulation levels of human
> and chimp brain *in vivo* and found them to be the same as *in vitro.* To
> put it another way it is not the amount of FOXP2 that made the difference in
> the gene regulation but the kind.
>
>
>> To control for any potential confounding effects of FOXP2 levels, we
>> performed correlations of the levels of every gene on the array to either
>> FOXP2 or FOXP2chimp levels, as well as performing random permutation
>> testing, and found no significant differences between other genes'
>> correlations to either FOXP2 or FOXP2chimp. These data indicate that the
>> differentially expressed genes are not due to different levels of FOXP2 or
>> FOXP2chimp, and are a true indication of differential transcriptional
>> regulation by these two proteins.
>>
>
> The conclusion of the paper is as follows (emphasis mine):
>
>
>> Using whole-genome microarrays, we uncovered genes that are differentially
>> regulated upon mutation of these two amino acids, including some with
>> functions critical to the development of the human central nervous system.
>> Moreover, this study reveals enrichment of differential FOXP2 targets with
>> known involvement in cerebellar motor function, craniofacial formation, and
>> cartilage and connective tissue formation, suggesting an important role for
>> human FOXP2 in establishing both the neural circuitry and physical
>> structures needed for spoken language. The significant overlap of human
>> FOXP2 targets in cell lines with genes enriched in human compared to
>> chimpanzee brain tissue presents the possibility that human and chimpanzee
>> FOXP2 have differentially regulated targets during brain development. As
>> suggested over 30 years ago24<http://www.nature.com/nature/journal/v462/n7270/full/nature08549.html#B24>,
>> and reaffirmed by the sequencing of both the human and chimpanzee genomes,
>> * the phenotypic differences exhibited by humans and chimpanzees cannot
>> be explained by differences in DNA sequence alone, and are probably due to
>> differences in gene expression and regulation*. Previous microarray
>> studies identified differences in gene expression between human and
>> chimpanzee brains25,
>> <http://www.nature.com/nature/journal/v462/n7270/full/nature08549.html#B25>
>> 26<http://www.nature.com/nature/journal/v462/n7270/full/nature08549.html#B26>.
>> Here, we link new whole-genome expression microarray data from human and
>> chimpanzee brain to direct differences in gene regulation by the human and
>> chimpanzee version of the transcription factor FOXP2. Because normal FOXP2
>> function is critical for speech in humans, these differentially regulated
>> targets may be relevant to the evolution and establishment or function of
>> pathways necessary for speech and language in humans.
>>
>
> The warp and woof of ID is that random mutation cannot generate the large
> changes found particularly between humans and other animals. Here we have a
> mere two amino acid change in a regulatory gene affects one characteristic
> that is quintessentially human, speech. A key characteristic of the
> mammalian genome versus other genomes is its "slower" evolution in the
> functional realm while "faster" evolution in the regulatory realm. The
> problem as I see it is the ID proponents oversimplify greatly the way random
> mutation works. This is not to say that this change is or is not guided.
> This "innovation" of the regulatory genes in the mammalian genome could very
> well be guided but we simply cannot tell from a scientific standpoint. For
> example, God may have guided the development of a placenta by allowing for a
> germ line retroviral infection long ago which in turn allowed for embryo
> implantation. See
> http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6W9P-45WPH5X-22&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=4aba222c919f82ab257a61442f826f2f.
>
> But how are we to "detect" this guidance? It's a lot more complicated
> than taking the odds of a single functional gene mutation and arbitrarily
> squaring them like Michael Behe does. Critics of ID like myself have noted
> that science cannot determine the guidance question one way or the other and
> by granting science this power you hand atheists such as Richard Dawkins a
> *huge* weapon. With the release of this paper today it just went up
> another notch because people like Dawkins can conclude that "science" has
> answered the speech question through "unguided" evolution.
>
> Rich Blinne
> Member ASA
>

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Received on Thu Nov 12 15:09:00 2009