Good Entropy

Nature, nurture and noise » Gene Expression

The basic problem with the interpretation above is that it limits “innate” influences to “genetic” ones. Just because some trait is not genetic does not mean it is not innate. If we are talking about how the brain gets wired, any number of prenatal environmental factors are known to have large effects. More interestingly, however, and probably a greater source of variance across the population, is intrinsic developmental variation. Wiring the brain is a highly complex procedure, reliant on cellular processes that are, in engineering terms, inherently “noisy”. Running the programme from the same starting point (a specific genotype) does not generate exactly the same output (the phenotype) every time. The effects of this noise are readily apparent at the anatomical level, when examining the impact of specific mutations, for example. In many cases, the phenotypic consequences are quite variable between genetically identical organisms, or even on two sides of the same brain. (If you want to see direct evidence of such developmental variation, take a directly face-on photograph of yourself, cut it in half and make mirror-image copies of the left and right sides. You will be amazed how different the two resultant faces are).

From Mounting evidence links language pathway to autism

FOXP2 codes for a protein that regulates the expression of other genes. Last year, an international group of scientists identified one of its targets, contactin-associated protein-like 2 (CNTNAP2). They also found that certain common variants of CNTNAP2 tend to crop up in people with specific language impairment, a developmental disorder.

CNTNAP2 was an exciting find because three independent teams had recently published that common variants of the gene up the risk of developing autism.

“I think the evidence now that CNTNAP2 is involved [in autism] is quite good,” says leader of one of the teams, Aravinda Chakravarti, professor at the McKusick Nathans Institute of Genetic Medicine at Johns Hopkins University. “We’re now interested in finding the molecular basis of this.”

In unpublished data, Chakravarti says he’s found that CNTNAP2 is over-expressed in a small number of postmortem autistic brains.

Geneticists have discovered many different autism-related variants of CNTNAP2, a massive gene spanning 2.3 million base pairs. “Disruptions in the front end of the gene [usually] mean you’ll get a more severe disorder, like full-blown autism or severe expressive language delay,” notes Martin Poot, research associate professor of medical genetics at the University Medical Center Utrecht, in the Netherlands.

The series of posts by these three authors illustrates, in microcosm, the melange of criticism commonly marshaled against mainstream science on intelligence in order to seem to discredit it without actually engaging its large interlocking body of evidence. Indeed, the criticism succeeds precisely by avoiding such engagement. There are two general strategies for avoiding the totality of relevant evidence: (1) create doubt about some small portion of it as if that isolated doubt nullified the totality of evidence, and (2) put unwelcome evidence off-limits by labeling it immoral or ill-motivated.

The game here is not to suppress discussion of genetic differences but to suppress knowledge of phenotypic differences. The latter make the former more plausible, so the specter of genetic causation is used as a club to beat back scientific knowledge about racial disparities in developed abilities, whatever their origins.

Original Article here
More thoughts by Linda S. Gottfredson

from The IQ Conundrum at Cato Unbound

FOXP2 and the Evolution of Language

This article addresses the history and the significance of the discovery of the relevance of FOXP2 in the development of speech. It is a remarkable scientific detective story that has been in the making for some time. In its earlier stages, there was serious disagreement within the scientific community about how the scientific findings should be interpreted, and this was set against a background of sensationalist reporting by the popular press.

and further on…

Human mind needs human cognition and human cognition relies on human speech. We cannot envisage humanness without the ability to think abstractly, but abstract thought requires language. This finding confirms that the molecular basis for the origin of human speech and, indeed, the human mind, is critical. Ultimately, we will find great insight from further unravelling the evolutionary roots of human speech – in contrast to Noam Chomsky’s lack of interest in this subject