Biophysics Unit, Department of Biochemistry and Molecular Biology, School of Medicine, and Center for Biophysic Studies, Universitat Autonoma de Barcelona, Bellaterra, Catalonia, Spain.
J Biol Chem. 2010 Aug 20;285(34):26431-40. doi: 10.1074/jbc.M110.138669. Epub 2010 Jun 10.
In eukaryotic cells a surveillance mechanism, the S phase checkpoint, detects and responds to DNA damage and replication stress, protecting DNA replication and arresting cell cycle progression. We show here that the S phase cyclins Clb5 and Clb6 are regulated in response to genotoxic stress in the budding yeast Saccharomyces cerevisiae. Clb5 and Clb6 are responsible for the activation of the specific Cdc28 cyclin-dependent kinase activity that drives the onset and progression of the S phase. Intriguingly, Clb5 and Clb6 are regulated by different mechanisms. Thus, the presence of Clb6, which is eliminated early in an unperturbed S phase, is stabilized when replication is compromised by replication stress or DNA damage. Such stabilization depends on the checkpoint kinases Mec1 and Rad53. The stabilization of Clb6 levels is a dynamic process that requires continued de novo protein synthesis, because the cyclin remains subject to degradation. It also requires the activity of the G(1) transcription factor Mlu1 cell cycle box-binding factor (MBF) in the S phase, whereas Dun1, the checkpoint kinase characteristically responsible for the transcriptional response to genotoxic stress, is dispensable in this case. On the other hand, two subpopulations of endogenous Clb5 can be distinguished according to turnover in an unperturbed S phase. In the presence of replication stress, the unstable Clb5 pool is stabilized, and such stabilization requires neither MBF transcriptional activity nor de novo protein synthesis.
在真核细胞中,有一种监控机制称为 S 期检查点,可以检测和响应 DNA 损伤和复制应激,从而保护 DNA 复制并阻止细胞周期进程。我们在这里表明,在芽殖酵母酿酒酵母中,细胞周期蛋白 Clb5 和 Clb6 会响应遗传毒性应激而受到调节。Clb5 和 Clb6 负责激活特定的 Cdc28 细胞周期蛋白依赖性激酶活性,该活性驱动 S 期的起始和进展。有趣的是,Clb5 和 Clb6 受到不同机制的调节。因此,在未受干扰的 S 期早期消除的 Clb6 的存在,在复制受到复制应激或 DNA 损伤的影响时会稳定下来。这种稳定依赖于检查点激酶 Mek1 和 Rad53。Clb6 水平的稳定是一个动态过程,需要持续的从头合成蛋白质,因为该细胞周期蛋白仍然容易被降解。它还需要 G1 转录因子 Mlu1 细胞周期盒结合因子(MBF)在 S 期的活性,而在这种情况下,通常负责对遗传毒性应激的转录反应的 Dun1 是可有可无的。另一方面,可以根据未受干扰的 S 期的周转率区分两种内源性 Clb5 亚群。在存在复制应激的情况下,不稳定的 Clb5 池被稳定下来,这种稳定既不需要 MBF 转录活性,也不需要从头合成蛋白质。