Abstract
they found that 80% of these DNAbinding regulatory sites were active during fetal development. Stamatoyannopoulos explained that the findings suggest there may be hundreds of thousands of regulatory switches involved in common diseases or traits, each contributing only slightly to a trait. This insight suggests it will be necessary to analyze genetic changes associated with disease as a system. “The system of gene regulation is complex—there are lots of moving parts—but it’s not so complicated we can’t figure things out,” he said. Feinberg argued that scientists have, in fact, known for decades that gene regulation plays an important role in disease and that much of the non–geneencoding DNA plays either a regulatory or structural role. He cited the pioneering work of Francis Collins on the role of a mutation in a regulatory region of DNA in a benign condition called hereditary persistence of fetal hemoglobin (Collins FS et al. Nature. 1985;313[6000]:325-326). He said that the article by Maurano et al “reinforces what we knew—that much disease is caused by gene regulation rather than by genes themselves.”
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