Hou Ming-Chin, Wiley David J, Verde Fulvia, McCollum Dannel
Department of Molecular Genetics and Microbiology, University of Massachusetts Medical School, Worcester, MA 01605, USA.
J Cell Sci. 2003 Jan 1;116(Pt 1):125-35. doi: 10.1242/jcs.00206.
The molecular mechanisms that temporally and spatially coordinate cell morphogenesis with the cell cycle remain poorly understood. Here we describe the characterization of fission yeast Mob2p, a novel protein required for regulating cell polarity and cell cycle control. Deletion of mob2 is lethal and causes cells to become spherical, with depolarized actin and microtubule cytoskeletons. A decrease in Mob2p protein level results in a defect in the activation of bipolar growth. This phenotype is identical to that of mutants defective in the orb6 protein kinase gene, and we find that Mob2p physically interacts with Orb6p. In addition, overexpression of Mob2p, like that of Orb6p, results in a delay in the onset of mitosis. Mob2p localizes to the cell periphery and cytoplasm throughout the cell cycle and to the division site during late anaphase and telophase. Mob2p is unable to localize to the cell middle in mutants defective in actomyosin ring and septum formation. Our results suggest that Mob2p, along with Orb6p, is required for coordinating polarized cell growth during interphase with the onset of mitosis.
在时间和空间上协调细胞形态发生与细胞周期的分子机制仍知之甚少。在此，我们描述了裂殖酵母Mob2p的特性，它是一种调节细胞极性和细胞周期控制所需的新型蛋白质。mob2基因的缺失是致死性的，并导致细胞变成球形，肌动蛋白和微管细胞骨架去极化。Mob2p蛋白水平的降低导致双极生长激活缺陷。这种表型与orb6蛋白激酶基因缺陷的突变体相同，并且我们发现Mob2p与Orb6p发生物理相互作用。此外，Mob2p的过表达，与Orb6p一样，导致有丝分裂起始延迟。在整个细胞周期中，Mob2p定位于细胞周边和细胞质，在后期和末期定位于分裂位点。在肌动球蛋白环和隔膜形成缺陷的突变体中，Mob2p无法定位于细胞中部。我们的结果表明，Mob2p与Orb6p一起，是间期极化细胞生长与有丝分裂起始协调所必需的。
