Genome Instability and Carcinogenesis, CNRS-UPR3081, Aix-Marseille University, Marseille, France.
Cell Cycle. 2012 Jan 1;11(1):151-8. doi: 10.4161/cc.11.1.18542.
In budding yeast, the cortical structure formed by the septins is remodeled at the onset of mitotic exit and delineates a specialized compartment dedicated to cytokinesis. How this septin function is spatially and timely regulated remains poorly understood. In this study, we report a role of the anillin-like protein Bud4 in the formation and the disassembly of the double ring structure formed by the septins at the time of cytokinesis. Bud4 acts with Bud3 in this pathway and in parallel with septin phosphorylation by the p21-activated kinase Cla4 and the septin-dependent kinase Gin4. In addition, we show that the function of Bud4 is regulated by the cyclin-dependent protein kinase Cdk1, the master regulator of cell cycle progression. This result suggests that the Cdks, or a locally specific pool of the kinase, may have a role past mitotic exit.
在芽殖酵母中，由隔膜蛋白形成的皮质结构在有丝分裂退出时被重塑，并划定了一个专门的隔间，专门用于胞质分裂。这种隔膜蛋白功能的空间和时间调节仍然知之甚少。在这项研究中，我们报告了类似于肌球蛋白的蛋白 Bud4 在胞质分裂时形成和组装由隔膜蛋白形成的双环结构中的作用。Bud4 在这个途径中与 Bud3 一起作用，与由 p21 激活激酶 Cla4 和隔膜蛋白依赖性激酶 Gin4 磷酸化的隔膜蛋白平行作用。此外，我们还表明，Bud4 的功能受到细胞周期蛋白依赖性蛋白激酶 Cdk1 的调节，Cdk1 是细胞周期进程的主要调节因子。这一结果表明，Cdk 或激酶的局部特定池可能在有丝分裂退出后发挥作用。
