New Characteristics of Drosophila Mutation RAD(2)201G1: Epigenetic Transmission of a Repair Defect via Meiosis and Association with the RadSIC gene

摘要

Current studies on double-strand DNA breaks (DSBs), which are the severest DNA damage in eukary-otes have demonstrated previously unknown relationships between breakage repair and chromatin, As shown for both mouse and human cells, the earliest cell response to DNA DSBs includes phosphorylation of H2AX histones, which precedes the formation of repair foci Rad.50, Rad.51, and Brcal. This process is controlled by gene ATM, mutations of which inhibit almost completely the formation of the above foci, although the products of respective repair genes are available in cells. These data suggest that genetically controlled changes in chromatin play a substantial regulatory role in DSB repair. Therefore, of interest are other mutations whose effects on DSB repair depend on chromatin properties.