Koyano Takayuki, Kume Kazunori, Konishi Manabu, Toda Takashi, Hirata Dai
Department of Molecular Biotechnology, Graduate School of Advanced Sciences of Matter, Hiroshima University, Higashi-Hiroshima, Japan.
Biosci Biotechnol Biochem. 2010;74(5):1129-33. doi: 10.1271/bbb.100223.
In eukaryotes, cell polarity is essential for cell proliferation, differentiation, and development. It is regulated in 3 steps: establishment, maintenance, and transition. Compared to current knowledge of establishment and maintenance, the mechanism regulating the transition of cell polarity is poorly understood. In fission yeast during the G2 phase, growth polarity undergoes a dramatic transition, from monopolar to bipolar growth (termed NETO: new end take off). In this study, we screened systematically for protein kinases related to NETO using a genome-wide kinase deletion library. Analysis of these deletions suggested that 35 and 2 kinases had a putative positive and a negative role, respectively, in NETO. Moreover, 5 kinases were required for NETO-delay in the G1-arrested cdc10 mutant. These results suggest that many signaling pathways are involved in the regulation of NETO.
在真核生物中,细胞极性对于细胞增殖、分化和发育至关重要。它通过三个步骤进行调节:建立、维持和转变。与目前关于建立和维持的知识相比,调节细胞极性转变的机制尚不清楚。在裂殖酵母的G2期,生长极性会经历从单极生长到双极生长的剧烈转变(称为NETO:新端起始)。在本研究中,我们使用全基因组激酶缺失文库系统地筛选了与NETO相关的蛋白激酶。对这些缺失的分析表明,分别有35种和2种激酶在NETO中具有假定的正向和负向作用。此外,在G1期停滞的cdc10突变体中,NETO延迟需要5种激酶。这些结果表明,许多信号通路参与了NETO的调节。