Role for the silencing protein Dot1 in meiotic checkpoint control
Role for the silencing protein Dot1 in meiotic checkpoint control
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DOI：
10.1091/mbc.11.10.3601
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发表时间：
2000-10-01
影响因子：
3.3
通讯作者：
Roeder, GS
中科院分区：
文献类型：
--
作者：
San-Segundo, PA;Roeder, GS
在减数分裂细胞周期中，一种称为“粗线期检查点”的监视机制通过在重组和染色体突触有缺陷时阻止减数分裂进程来确保正确的染色体分离。沉默蛋白Dot 1（也称为Pch 1）是酿酒酵母zip1和dmc 1突变体的检查点介导的粗线期阻滞所必需的。在没有DOT 1的情况下，zip1和dmc 1突变体不适当地通过减数分裂进行，产生不可活的减数分裂产物。粗线期检查点的其他组分包括核仁蛋白Pch 2和异染色质组分Sir 2。在dot1中，检查点的破坏与核仁中Pch 2和Sir 2浓度的损失相关。除了它的检查点功能，Dot1阻断了通过Rad54依赖的姐妹染色单体之间重组途径修复减数分裂双链断裂。在营养细胞中，DOT 1的突变导致Sir 3从端粒中离域，从而导致DOT 1中端粒沉默受损。
During the meiotic cell cycle, a surveillance mechanism called the "pachytene checkpoint" ensures proper chromosome segregation by preventing meiotic progression when recombination and chromosome synapsis are defective. The silencing protein Dot1 (also known as Pch1) is required for checkpoint-mediated pachytene arrest of the zip1 and dmc1 mutants of Saccharomyces cerevisiae. In the absence of DOT1, the zip1 and dmc1 mutants inappropriately progress through meiosis, generating inviable meiotic products. Other components of the pachytene checkpoint include the nucleolar protein Pch2 and the heterochromatin component Sir2. In dot1, disruption of the checkpoint correlates with the loss of concentration of Pch2 and Sir2 in the nucleolus. In addition to its checkpoint function, Dot1 blocks the repair of meiotic double-strand breaks by a Rad54-dependent pathway of recombination between sister chromatids. In vegetative cells, mutation of DOT1 results in delocalization of Sir3 from telomeres, accounting for the impaired telomeric silencing in dot1.