Cooper Katrina F, Strich Randy
Program for Cell and Developmental Biology, Fox Chase Cancer Center, Philadelphia, Pennsylvania 19111, USA.
Eukaryot Cell. 2002 Feb;1(1):66-74. doi: 10.1128/EC.01.1.66-74.2002.
The yeast C-type cyclin Ume3p/Srb11p and its cyclin-dependent kinase partner Ume5p/Srb10p repress the transcription of several genes required for meiotic recombination or meiosis I nuclear division. To relieve this repression, Srbllp is destroyed early in meiosis, prior to the first meiotic division. This report identifies two roles for Srb11p in regulating meiotic development. First, SRB11 is required for the normal exit from the mitotic cell cycle prior to meiotic induction. Specifically, mutants lacking SRB11 (srb11delta) uncouple bud growth from chromosome segregation, producing small buds with nuclei. The bud growth defect is most likely due to the failure of srb11delta mutants to reestablish polarized actin fibers at the bud tip following exposure to sporulation medium. Second, Srb11p is required for the efficient execution of meiosis I. srb11delta mutants either exhibited a delay in performing meiosis I and meiosis II or skipped meiosis I entirely. This meiotic defect is not due to the activation of the recombination or spindle assembly checkpoint pathways. However, the expression of several meiotic genes is delayed and reduced in the mutant strains. These results suggest a positive role for Srb10-Srb11p in regulating the transcription program. This model is supported by the finding that overexpression of the meiotic inducer IME2 partially restored the ability of srb11 mutants to perform meiosis I. In conclusion, these findings indicate that Srb11p is required for both entry into and execution of the meiotic program, thus describing multiple roles for a C-type cyclin in the regulation of a developmental pathway.
酵母C型细胞周期蛋白Ume3p/Srb11p及其细胞周期蛋白依赖性激酶伴侣Ume5p/Srb10p抑制减数分裂重组或减数分裂I核分裂所需的几个基因的转录。为了解除这种抑制,Srbllp在减数分裂早期、第一次减数分裂之前被破坏。本报告确定了Srb11p在调节减数分裂发育中的两个作用。首先,SRB11是减数分裂诱导前正常退出有丝分裂细胞周期所必需的。具体而言,缺乏SRB11的突变体(srb11delta)使芽生长与染色体分离解偶联,产生带有细胞核的小芽。芽生长缺陷很可能是由于srb11delta突变体在暴露于孢子形成培养基后未能在芽尖重新建立极化的肌动蛋白纤维。其次,Srb11p是有效执行减数分裂I所必需的。srb11delta突变体要么在进行减数分裂I和减数分裂II时出现延迟,要么完全跳过减数分裂I。这种减数分裂缺陷不是由于重组或纺锤体组装检查点途径的激活。然而,几个减数分裂基因的表达在突变菌株中延迟且减少。这些结果表明Srb10-Srb11p在调节转录程序中具有积极作用。减数分裂诱导剂IME2的过表达部分恢复了srb11突变体进行减数分裂I的能力,这一发现支持了该模型。总之,这些发现表明Srb11p是进入和执行减数分裂程序所必需的,从而描述了C型细胞周期蛋白在发育途径调节中的多种作用。