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A new layer of degradation mechanism for PR-Set7/Set8 during cell cycle

机译：细胞周期期间PR-Set7 / Set8的新降解机制层

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Set8 is critically involved in transcription regulation, cell cycle progression and genomic stability. Emerging evidence has revealed that E3 ubiquitin ligases such as CRL4cdt2 and SCFSkp2 regulate Set8 protein abundance. However, it is unclear whether other E3 ligase(s) could govern Set8 level for proper cell cycle progression in response to genotoxic stress such as UV irradiation. Recently, we report that the SCF beta-TRCP complex regulates Set8 protein stability by targeting it for ubiquitination and subsequent degradation. Notably, Set8 interacts with the SCF beta-TRCP E3 ligase complex. We further revealed a critical role of CKI in SCF beta-TRCP-mediated degradation of Set8. Mechanistically, CKI-mediated phosphorylation of Set8 at the S253 site promotes its destruction by SCF beta-TRCP. Importantly, SCF beta-TRCP-dependent Set8 destruction also contributes to the tight control of cell proliferation and cell cycle progression, in response to UV irradiation. Here, we summarize our new findings regarding the crucial role of beta-TRCP in CKI-mediated Set8 degradation, which could provide new evidence to support that dysregulation of a tight regulatory network of Set8 could lead to aberrant cell cycle process.
机译：Set8关键参与转录调节，细胞周期进程和基因组稳定性。新兴证据表明，E3泛素连接酶（例如CRL4cdt2和SCFSkp2）调节Set8蛋白的丰度。但是，尚不清楚其他E3连接酶是否可以控制Set8水平以响应遗传毒性应激（例如UV辐射）而使细胞周期正常进行。最近，我们报告说，SCF beta-TRCP复合物通过将其靶向泛素化和随后的降解来调节Set8蛋白的稳定性。值得注意的是，Set8与SCF beta-TRCP E3连接酶复合物相互作用。我们进一步揭示了CKI在SCFβ-TRCP介导的Set8降解中的关键作用。从机理上讲，在S253位点，CKI介导的Set8磷酸化促进了SCF beta-TRCP的破坏。重要的是，响应于紫外线照射，SCFβ-TRCP依赖性Set8破坏也有助于严格控制细胞增殖和细胞周期进程。在这里，我们总结了有关β-TRCP在CKI介导的Set8降解中的关键作用的新发现，这可能提供新的证据来支持Set8紧密调控网络的失调可能导致异常的细胞周期过程。

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