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

机译：在细胞周期中PR-Set7 / Set8的新一层劣化机制

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摘要

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批判性地参与转录调节，细胞周期进展和基因组稳定性。新兴的证据表明，E3泛素连接酶如CRL4CDT2和SCFSKP2调节SET8蛋白质丰富。然而，目前尚不清楚其他E3连接酶是否可以针对诸如UV辐射等遗传毒性应激的遗传毒性应激来治理适当的细胞周期进展。最近，我们认为SCFβ-TRCP复合体通过针对泛素化和随后的降解来调节SED8蛋白稳定性。值得注意的是，Set8与SCFβ-TRCP E3连接酶复合物交互。我们进一步揭示了CKI在SCFβ-TRCP介导的Set8降解中的关键作用。机械地，CKI介导的SED8在S253位点的磷酸化促进了SCFβ-TRCP的破坏。重要的是，依赖于紫外线照射，SCFβ-TRCP依赖的SET8破坏也有助于对细胞增殖和细胞周期进展的紧密控制。在这里，我们总结了关于β-TRCP在CKI介导的SET8降级中的关键作用的新发现，这可以提供新的证据来支持，支持Set8的紧张监管网络的失调可能导致异常的细胞周期过程。

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