ArticleCell cycle (Georgetown, Tex.)2013
A knockout screen for protein kinases required for the proper meiotic segregation of chromosomes in the fission yeast Schizosaccharomyces pombe.
Article in Cell cycle (Georgetown, Tex.), 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Quantitative proteomics and phosphoproteomics profiling of meiotic divisions in the fission yeast Schizosaccharomyces pombe.Scientific reports · 2024Article
- Sororin is an evolutionary conserved antagonist of WAPL.Nature communications · 2024Article
- Nickel induced cell impairments are negatively regulated by the Tor1 kinase in Schizosaccharomyces pombe.World journal of microbiology & biotechnology · 2021Article
- Review
- The Gpr1/Zdbf2 locus provides new paradigms for transient and dynamic genomic imprinting in mammals.Genes & development · 2014Article
- Mal3, the Schizosaccharomyces pombe homolog of EB1, is required for karyogamy and for promoting oscillatory nuclear movement during meiosis.Cell cycle (Georgetown, Tex.) · 2014Article
- Protein kinases required for proper segregation of chromosomes during meiosis.Cell cycle (Georgetown, Tex.) · 2013Article
- Phosphorylation: a key regulator of meiosis.Cell cycle (Georgetown, Tex.) · 2013Article
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8 authors at 3 institutions in 2 countries.
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Abstract
The reduction of chromosome number during meiosis is achieved by two successive rounds of chromosome segregation after just single round of DNA replication. To identify novel proteins required for the proper segregation of chromosomes during meiosis, we analyzed the consequences of deleting Schizosaccharomyces pombe genes predicted to encode protein kinases that are not essential for cell viability. We show that Mph1, a member of the Mps1 family of spindle assembly checkpoint kinases, is required to prevent meiosis I homolog non-disjunction. We also provide evidence for a novel function of Spo4, the fission yeast ortholog of Dbf4-dependent Cdc7 kinase, in regulating the length of anaphase II spindles. In the absence of Spo4, abnormally elongated anaphase II spindles frequently overlap and thus destroy the linear order of nuclei in the ascus. Our observation that the spo4Δ mutant phenotype can be partially suppressed by inhibiting Cdc2-as suggests that dysregulation of the activity of this cyclin-dependent kinase may cause abnormal elongation of anaphase II spindles in spo4Δ mutant cells.
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