Juanes M Angeles, Queralt Ethel, Bañó M Carmen, Igual J Carlos
Departament de Bioquímica i Biologia Molecular, Facultat de Ciències Biològiques, Universitat de València, 46100 Burjassot (Valencia), Spain.
J Cell Sci. 2007 Jul 15;120(Pt 14):2390-401. doi: 10.1242/jcs.002758.
ROT1 is an essential gene whose inactivation causes defects in cell cycle progression and morphogenesis in budding yeast. Rot1 affects the actin cytoskeleton during the cell cycle at two levels. First, it is required for the maintenance of apical growth during bud growth. Second, Rot1 is necessary to polarize actin cytoskeleton to the neck region at the end of mitosis; because of this defect, rot1 cells do not properly form a septum to complete cell division. The inability to polarize the actin cytoskeleton at the end of mitosis is not due to a defect in the recruitment of the polarisome scaffold protein Spa2 or the actin cytoskeleton regulators Cdc42 and Cdc24 in the neck region. Previous results indicate a connection between Rot1 and the cyclin Clb2. In fact, overexpression of CLB2 is toxic when ROT1 is partially inactivated, and reciprocally, deletion of CLB2 suppresses the lethality of the rot1 mutant, which indicates a functional antagonism between Clb2 and Rot1. Several genetic interactions suggest a link between Rot1 and the ubiquitin-proteasome system and we show that the Clb2 cyclin is not properly degraded in rot1 cells.
ROT1是一个必需基因，其失活会导致芽殖酵母细胞周期进程和形态发生出现缺陷。Rot1在细胞周期的两个层面影响肌动蛋白细胞骨架。首先，它是芽生长过程中顶端生长维持所必需的。其次，Rot1对于有丝分裂末期肌动蛋白细胞骨架向颈部区域极化是必需的；由于这个缺陷，rot1细胞不能正确形成隔膜来完成细胞分裂。有丝分裂末期肌动蛋白细胞骨架不能极化并非由于颈部区域极性体支架蛋白Spa2或肌动蛋白细胞骨架调节因子Cdc42和Cdc24募集缺陷所致。先前的结果表明Rot1与细胞周期蛋白Clb2之间存在联系。事实上，当ROT1部分失活时，CLB2的过表达具有毒性，反之，CLB2的缺失可抑制rot1突变体的致死性，这表明Clb2与Rot1之间存在功能拮抗作用。一些遗传相互作用表明Rot1与泛素-蛋白酶体系统之间存在联系，并且我们发现细胞周期蛋白Clb2在rot1细胞中不能被正确降解。
