Year: 2021
Type: preprint
Abstract: ABSTRACT Epigenetic mechanisms mediate diverse gene expression programs in growth and development. Here we report a protein-based epigenetic element, a prion, formed by the conserved DNA helicase Mph1/FANCM. [ MIX + ] is a cytoplasmically inherited state with propagation driven by the non-amyloid prion templating of Mph1. [ MIX + ] provides resistance to DNA damage, a gain-of-function trait that requires helicase activity. [ MIX + ] reduces mitotic mutation rates, but promotes meiotic crossovers, driving measurable phenotypic diversification in wild outcrosses. Remarkably, [ MIX + ] can be induced by DNA-damaging stresses in which it is beneficial. Thus, [ MIX + ] fuels a quasi-Lamarckian form of inheritance that promotes survival of the current generation and diversification of the next.
Institutions: Stanford Medicine, Stanford University, University of Oregon
Language: English
Topic: DNA Repair Mechanisms
Subfield: Molecular Biology
Domain: Life Sciences
Open Access status: green
OpenAlex ID: W3208340281