Which sense do you value the most? I think many people, if they had to choose, would stick to their vision as the must-have sense. One thing that I want to get beyond on this blog is the tendency to find the one-gene-that-causes-all phenomenon. This tendency to fix on genes of large and singular affect, traditional Mendelian phenotypes like cystic fibrosis (a recessive disease), has been dictated by the lack of power of and limitations in studying quantitative traits, where I think the real uncharted territory is going to be with the next few decades. Nevertheless, a new paper in Nature Genetics caught my eye, so to speak. The authors suggest that "...analysis of the C2 and BF haplotypes and CFH variants shows that variation in the two loci can predict the clinical outcome in 74% of the affected individuals and 56% of the controls." In short, the most common form of blindness in the modern world can be predicted to a large extent by two loci. This is a step beyond the one-gene-gene-that-causes-all narrative, as you have to take into account two locations on the genome, but it shows that relatively simple traits of interest are still around as "low hanging fruit."
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It's a shame that NIH funding is falling behind just as new technologies for doing human genetics easily are coming on-line.
You didn't want to be deaf before the days of sign language -- those born deaf lacked a way to think in words, so they were, in effect, mentally retarded. Thus, the two meanings of "dumb."
Single-gene explanations of problems are unexceptional. In any system, e.g. an automobile, it's possible to make it non-functional with a single change -- disconnecting a wire, closing a vent, removing a part. And a single change can repair it too.
Normal function, though, requires all the parts, not just one. So while you can bring a specific car from non-functioning to normal with a single change, that doesn't mean that that single thing changed is "the cause" of normal functioning. The whole car is the cause.
Thus a simple single-factor reductionist theory of defect is OK, and not reductionism at all. Single-factor explanations of normality or high function need much more examination.
It's ture that the superior functioning in some respect of A over B might be explained by a single factor -- the explanation of a difference, again. But the superior functioning requires not only the new factor unique to A, but also many of the many other factors common to A and B.
What's relevant here is that it is not a single gene, but a single pathway that appears to be responsible for a significant disease burden. Another related comment is that the disease is a very common one. The pathway also happens to be one susceptible to pharmacologic modulation. So, therapy may not be that far off. All in all, a pretty good argument for continuing genetic work on the mechanism of this common disease.