据研究人员介绍，细胞分裂被认为是由细胞周期蛋白依赖性激酶（Cdk）失活关键的转录抑制剂而启动的。在出芽酵母中，G1细胞周期蛋白Cln3-Cdk1复合体被认为能直接磷酸化Whi5蛋白，从而释放转录因子SBF并使细胞进入分裂。
研究人员发现，Whi5是Cln3-Cdk1的一个弱底物，相反，它将RNA聚合酶II亚基Rpb1的C端域磷酸化在其七肽重复序列的S5上。Cln3-Cdk1结合SBF调控的启动子，Cln3的功能可由典型的S5激酶Ccl1-Kin28在合成招募到SBF时执行。因此，研究人员提出Cln3-Cdk1通过在SBF调控的启动子上磷酸化Rpb1，从而促进转录来触发细胞分裂。这个发现模糊了细胞周期和转录Cdk之间的区别，并突出了这两个过程之间的古老关系。
附：英文原文
Title: G1 cyclin–Cdk promotes cell cycle entry through localized phosphorylation of RNA polymerase II
Author: Mardo Kivomgi, Matthew P. Swaffer, Jonathan J. Turner, Georgi Marinov, Jan M. Skotheim
Issue&Volume: 2021-10-15
Abstract: Cell division is thought to be initiated by cyclin-dependent kinases (Cdks) inactivating key transcriptional inhibitors. In budding yeast, the G1 cyclin Cln3-Cdk1 complex is thought to directly phosphorylate the Whi5 protein, thereby releasing the transcription factor SBF and committing cells to division. We report that Whi5 is a poor substrate of Cln3-Cdk1, which instead phosphorylates the RNA polymerase II subunit Rpb1’s C-terminal domain on S5 of its heptapeptide repeats. Cln3-Cdk1 binds SBF-regulated promoters and Cln3’s function can be performed by the canonical S5 kinase Ccl1-Kin28 when synthetically recruited to SBF. Thus, we propose that Cln3-Cdk1 triggers cell division by phosphorylating Rpb1 at SBF-regulated promoters to promote transcription. Our findings blur the distinction between cell cycle and transcriptional Cdks to highlight the ancient relationship between these two processes.
DOI: aba5186
Source: https://www.science.org/doi/10.1126/science.aba5186