Epigenesis: the missing beat in biotechnology?
The range of human phenotypes/diseases for which our burgeoning bio-molecular data base is sufficient to provide understanding, diagnosis, and therapy is small. Only 2 percent of our total disease load is related to monogenic causality, and even here the final phenotype is modulated by many factors. Monogenic logic cannot, moreover, be applied to the 98 percent of our most important sources of premature disability and death. This article provides an analysis of the limits of genetic thinking in biotechnology and describes the outline for another approach to understanding complex cellular/physiological systems. In this outline, rules governing physiological regulation and cellular and higher levels of organization are located not in the genome, but in interactive epigenetic networks which themselves organize genomic response to environmental signaling.
Strohman
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Department of Molecular & Cell Biology, University of California, Berkeley 94720.
D000818:Animals; D001709:Biotechnology; D003866:Depressive Disorder / Q000235:genetics; D030342:Genetic Diseases, Inborn / Q000175:diagnosis / Q000235:genetics*; D005826:Genetics, Medical; D006801:Humans; D006973:Hypertension / Q000175:diagnosis / Q000235:genetics; D008967:Molecular Biology; D009203:Myocardial Infarction / Q000175:diagnosis / Q000235:genetics; D009369:Neoplasms / Q000235:genetics; D012559:Schizophrenia / Q000235:genetics