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- W3045528065 endingPage "766" @default.
- W3045528065 startingPage "752" @default.
- W3045528065 abstract "In germ cells undergoing meiosis, the induction of double strand breaks (DSBs) is required for the generation of haploid gametes. Defects in the formation, detection, or recombinational repair of DSBs often result in defective chromosome segregation and aneuploidies. Central to the ability of meiotic cells to properly respond to DSBs are DNA damage response (DDR) pathways mediated by DNA damage sensor kinases. DDR signaling coordinates an extensive network of DDR effectors to induce cell cycle arrest and DNA repair, or trigger apoptosis if the damage is extensive. Despite their importance, the functions of DDR kinases and effector proteins during meiosis remain poorly understood and can often be distinct from their known mitotic roles. A key DDR kinase during meiosis is ataxia telangiectasia and Rad3-related (ATR). ATR mediates key signaling events that control DSB repair, cell cycle progression, and meiotic silencing. These meiotic functions of ATR depend on upstream scaffolds and regulators, including the 9-1-1 complex and TOPBP1, and converge on many downstream effectors such as the checkpoint kinase CHK1. Here, we review the meiotic functions of the 9-1-1/TOPBP1/ATR/CHK1 signaling pathway during mammalian meiosis." @default.
- W3045528065 created "2020-08-03" @default.
- W3045528065 creator A5025725461 @default.
- W3045528065 creator A5050632141 @default.
- W3045528065 creator A5074190295 @default.
- W3045528065 creator A5078982458 @default.
- W3045528065 date "2020-08-01" @default.
- W3045528065 modified "2023-10-17" @default.
- W3045528065 title "ATR signaling in mammalian meiosis: From upstream scaffolds to downstream signaling" @default.
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