The more closely geneticists look at complex traits and diseases, the harder it gets to find active genes that don’t influence them.
From Veronique Greenwood at Quanta:
Mutations of a single gene are behind sickle cell anemia, for instance, and mutations in another are behind cystic fibrosis.
But unfortunately for those who like things simple, these conditions are the exceptions. The roots of many traits, from how tall you are to your susceptibility to schizophrenia, are far more tangled. In fact, they may be so complex that almost the entire genome may be involved in some way…
One very early genetic mapping study in 1999 suggested that “a large number of loci (perhaps > than 15)” might contribute to autism risk, recalled Jonathan Pritchard, now a geneticist at Stanford University. “That’s a lot!” he remembered thinking when the paper came out.
Over the years, however, what scientists might consider “a lot” in this context has quietly inflated. Last June, Pritchard and his Stanford colleagues Evan Boyle and Yang Li (now at the University of Chicago) published a paper about this in Cell that immediately sparked controversy, although it also had many people nodding in cautious agreement. The authors described what they called the “omnigenic” model of complex traits. Drawing on GWAS analyses of three diseases, they concluded that in the cell types that are relevant to a disease, it appears that not 15, not 100, but essentially all genes contribute to the condition. The authors suggested that for some traits, “multiple” loci could mean more than 100,000. More.
This isn’t the Darwinism we were promised.
Hat tip: Philip Cunningham
See also: New book from Michael Behe on how today’s DNA findings “devolve” Darwin. Devolution… at last, something Darwinism really explains! How odd that genome mapper and theistic evolutionist Francis Collins should have helped kill Darwinism before he got most Christians to buy into it.