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

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 13:18:29 2009