DNA double-strand break-induced phosphorylation of Drosophila histone variant H2Av helps prevent radiation-induced apoptosis.

摘要: The response of eukaryotic cells to the formation a double-strand break (DSB) in chromosomal DNA is highly conserved. One earliest responses DSB phosphorylation C-terminal tail H2A histones located nucleosomes near break. Histone variant H2AX and core histone are phosphorylated mammals budding yeast, respectively. We demonstrate DSB-induced H2Av Drosophila melanogaster. member H2AZ family variants. Ser137 within an SQ motif C- terminus was γ-irradiation both tissue culture larvae. Phosphorylation detected 1 min irradiation detectable after only 0.3 Gy radiation exposure. Photochemically induced DSBs, but not general oxidative damage or UV-induced nicking DNA, caused phosphorylation, suggesting that specific. Imaginal disc from expressing mutant allele with its deleted, therefore unable be phosphorylated, were more sensitive radiation-induced apoptosis than wildtype controls, important for repair DSBs. These observations suggest addition providing function histone, also functional homolog H2AX.