Biosignal Research Center, Kobe University, 1-1, Rokkodai-cho, Nada-ku, Kobe 657-8501, Japan.
Department of Pharmaceutical Sciences, University of Shizuoka, 52-1 Yada, Suruga-ku, Shizuoka 422-8526, Japan.
Biomolecules. 2021 Jan 12;11(1):89. doi: 10.3390/biom11010089.
Meiosis is a specialized cell division process that mediates genetic information transfer to the next generation. Meiotic chromosomal segregation occurs when DNA replication is completed during the pre-meiotic S phase. Here, we show that Pef1, an orthologue of mammalian cyclin-dependent kinase 5 (CDK5), is required to promote pre-meiotic DNA replication. We examined the efficiency of meiotic initiation using mutants and found that, meiotic nuclear divisions did not occur in the strain. Deletion of also suppressed the expression of DNA replication factors and the phosphorylation of Cdc2 Tyr-15. The double deletion of and arrested meiotic initiation in mutant cells, similar to that of -deficient cells. Meiotic progression was also slightly delayed in the -deficient strain. Our results reveal that Pef1 regulates cyclin-coordinated meiotic progression.
减数分裂是一种介导遗传信息传递到下一代的特殊细胞分裂过程。减数分裂中的染色体分离发生在预减数分裂 S 期,此时 DNA 复制完成。在这里,我们表明 Pef1,一种与哺乳动物细胞周期蛋白依赖性激酶 5 (CDK5) 同源的蛋白,是促进预减数分裂 DNA 复制所必需的。我们使用 突变体检查了减数分裂起始的效率,发现 突变体中没有发生减数分裂核分裂。删除 也抑制了 DNA 复制因子的表达和 Cdc2 Tyr-15 的磷酸化。 和 的双重缺失使 突变体细胞中的减数分裂起始停滞,类似于 -缺陷细胞。在 -缺陷菌株中,减数分裂进程也略有延迟。我们的结果表明,Pef1 调节细胞周期协调的减数分裂进程。