Abstract
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 Schizosaccharomyces pombe 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 pat1-114 mutants and found that, meiotic nuclear divisions did not occur in the pef1Δ pat1-114 strain. Deletion of pef1 also suppressed the expression of DNA replication factors and the phosphorylation of Cdc2 Tyr-15. The double deletion of clg1 and psl1 arrested meiotic initiation in pat1-114 mutant cells, similar to that of pef1-deficient cells. Meiotic progression was also slightly delayed in the pas1-deficient strain. Our results reveal that Pef1 regulates cyclin-coordinated meiotic progression.
Highlights
Sexual reproduction is an important process that mediates genetic information transfer to the generation in many species, including yeast and mammals
Gametes form through meiotic cell division, which is accomplished by DNA synthesis, during the premeiotic S phase followed by two consecutive rounds of nuclear division
Using pat1-114 temperature-sensitive mutant strains, which can induce meiosis by shifting the permissive temperature (25 ◦ C) to a restrictive temperature (34 ◦ C), we reveal that Pef1 is required for Cdc2 Tyr-15 phosphorylation and DNA replication during the pre-meiotic S phase
Summary
Sexual reproduction is an important process that mediates genetic information transfer to the generation in many species, including yeast and mammals. Gametes form through meiotic cell division, which is accomplished by DNA synthesis, during the premeiotic S phase followed by two consecutive rounds of nuclear division (meiosis I and meiosis II). Meiosis results in gene diversity in gametes primarily through homologous recombination at specific genome regions known as ‘hot spots.’. Homologous recombination takes place due to repair of DNA damage caused by self-inflicted double-strand breaks (DSBs) [1]. In response to the accumulated unrepaired DSBs, checkpoint machinery arrests or delays the meiotic cell cycle, preventing misregulation of chromosomal segregation. Precise DNA replication and DSB repair are essential for initiating meiotic nuclear division [2]
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