ATR signaling in mammalian meiosis: From upstream scaffolds to downstream signaling.
ATR signaling in mammalian meiosis: From upstream scaffolds to downstream signaling.
复制标题
哺乳动物减数分裂中的ATR信号传导：从上游支架到下游信号传导。
DOI：
10.1002/em.22401
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发表时间：
2020-08
影响因子：
2.8
通讯作者：
Brieño-Enríquez MA
中科院分区：
文献类型：
--
作者：
Pereira C;Smolka MB;Weiss RS;Brieño-Enríquez MA
在经历减数分裂的生殖细胞中，单倍体配子的产生需要诱导双链断裂（DSB）。 DSB 形成、检测或重组修复中的缺陷通常会导致染色体分离缺陷和非整倍体。减数分裂细胞对 DSB 做出正确反应的能力的核心是由 DNA 损伤传感器激酶介导的 DNA 损伤反应 (DDR) 途径。 DDR 信号传导协调广泛的 DDR 效应器网络，诱导细胞周期停滞和 DNA 修复，或者在损伤广泛时触发细胞凋亡。尽管很重要，但 DDR 激酶和效应蛋白在减数分裂过程中的功能仍然知之甚少，并且通常与其已知的有丝分裂作用不同。减数分裂期间的关键 DDR 激酶是毛细血管扩张共济失调和 Rad3 相关 (ATR)。 ATR 介导控制 DSB 修复、细胞周期进程和减数分裂沉默的关键信号传导事件。 ATR 的这些减数分裂功能依赖于上游支架和调节因子，包括 9-1-1 复合体和 TOPBP1，并汇聚于许多下游效应子，例如检查点激酶 CHK1。在这里，我们回顾了哺乳动物减数分裂过程中9-1-1/TOPBP1/ATR/CHK1信号通路的减数分裂功能。
In germ cells undergoing meiosis, the induction of double strand breaks (DSB) is required for the generation of haploid gametes. Defects in the formation, detection or recombinational repair of DSB 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.
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影响因子：
16.8
作者：
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通讯作者：
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影响因子：
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