Rad9B responds to nucleolar stress through ATR and JNK signalling, and delays the G1-S transition
Rad9B responds to nucleolar stress through ATR and JNK signalling, and delays the G1-S transition
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DOI：
10.1242/jcs.091124
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发表时间：
2012-03-01
影响因子：
4
通讯作者：
Freire, Raimundo
中科院分区：
文献类型：
--
作者：
Jesus Perez-Castro, Antonio;Freire, Raimundo
Rad9、Rad1和Hus1（9-1-1）组成的复合物通过激活DNA损伤检查点和DNA损伤修复途径来防止基因组不稳定，主要是在复制分叉崩溃和紫外线损伤的反应中。在这里，我们比较了Rad9A（也称为Rad9）与人类对话Rad9B的作用。与Rad9A不同，过表达Rad9B会使细胞在G1期延迟。此外，Rad9B在核仁胁迫后以atr和jnk依赖的方式迁移到核仁，这是一种新描述的含有p21的核仁结构域结构。Rad9A和Rad9B嵌合体的分析表明，在核仁上的定位和过表达后G1期的阻滞主要依赖于Rad9B的c端尾部。综上所述，本文提供的数据显示了Rad9B与检查点通路、应激反应和核核功能之间的关系。
The complex formed by Rad9, Rad1 and Hus1 (9-1-1) protects against genomic instability by activating DNA damage checkpoint and DNA damage repair pathways, mainly in response to replication fork collapse and UV lesions. Here we compare the role of Rad9A (also known as Rad9) with the human paralogue Rad9B. Unlike Rad9A, overexpression of Rad9B delays cells in G1 phase. Moreover, Rad9B migrates to nucleoli after nucleolar stress in an ATR-and JNK-dependent manner, in a newly described nucleolar domain structure containing p21. Analysis of chimeras of Rad9A and Rad9B demonstrate that localisation to nucleoli and the block in G1 phase upon overexpression crucially depend on the Rad9B C-terminal tail. Taken together, data presented here show a relationship between Rad9B and pathways for checkpoints, stress response and nucleolar function.