作者: Jasmine Siler , Na Guo , Zhengfeng Liu , Yuhua Qin , Xin Bi
DOI: 10.1101/572271
关键词:
摘要: DNA lesions trigger the activation of damage checkpoints (DDCs) that stop cell cycle progression and promote repair. Saccharomyces cerevisiae Tel1 is a homolog mammalian ATM kinase plays an auxiliary role in DDC signaling. {gamma}H2A, equivalent to {gamma}H2AX mammals, early chromatin mark induced by recognized group repair factors. We find both {gamma}H2A negatively impact G2/M checkpoint response topoisomerase I poison camptothecin independently each other. also regulates alkylating agent methyl methanesulfonate. These results, together with prior findings demonstrating positive or no roles other damaging agents such as phleomycin ionizing radiation, suggest have damage-specific effects on DDC. present data indicating acts same pathway Mre11-Rad50-Xrs2 complex suppress CPT possibly repairing I-DNA crosslink. On hand, we evidence consistent notion mediating competitive recruitment mediator Rad9 factor Rtt107 sites damage. propose serves create dynamic balance between influenced nature