Saka Y, Yanagida M
Department of Biophysics, Faculty of Science, Kyoto University, Japan.
Cell. 1993 Jul 30;74(2):383-93. doi: 10.1016/0092-8674(93)90428-s.
Fission yeast cut5 mutants cause cytokinesis in the absence of normal nuclear division. We show here that cut5+ is required for both the onset of S phase and the restraint of M phase before the completion of S phase. The primary defects in cut5 mutants occur prior to S phase, but cells suffer lethal damage during M phase. Mitosis and cytokinesis occur in the presence of hydroxyurea or in the double mutant cdc10-cut5 (the cdc10 mutation alone blocks progression from G1 to S). Gene cloning shows that cut5+ is identical to the fission yeast rad4+ gene, which is similar to human XRCC1. The rad4+/cut5+ gene is unique in its positive role for replication/repair and in its negative role for mitosis/cytokinesis. We propose a single/twin chromatid marking model for rad4+/cut5+ function in cell cycle control.
裂殖酵母cut5突变体在没有正常核分裂的情况下引发胞质分裂。我们在此表明,cut5+对于S期的起始以及在S期完成之前对M期的抑制都是必需的。cut5突变体的主要缺陷发生在S期之前,但细胞在M期会遭受致命损伤。在存在羟基脲的情况下或在双突变体cdc10 - cut5(单独的cdc10突变会阻断从G1期到S期的进程)中会发生有丝分裂和胞质分裂。基因克隆表明,cut5+与裂殖酵母rad4+基因相同,后者与人类XRCC1相似。rad4+/cut5+基因在复制/修复方面的正向作用以及在有丝分裂/胞质分裂方面的负向作用是独特的。我们提出了一个关于rad4+/cut5+在细胞周期调控中功能的单/双染色单体标记模型。