ArticlePloS one2012
Yeast IME2 functions early in meiosis upstream of cell cycle-regulated SBF and MBF targets.
Article in PloS one, 2012. 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, 12 citations in OpenAlex.
- Response mechanisms of different Saccharomyces cerevisiae strains to succinic acid.BMC microbiology · 2024Article
- Article
- Vir1p, the yeast homolog of virilizer, is required for mRNA m6A methylation and meiosis.Genetics · 2023Article
- Vir1p, the Yeast Homolog of Virilizer, is Required for mRNA mbioRxiv : the preprint server for biology · 2023Article
- Phospho-Regulation of Meiotic Prophase.Frontiers in cell and developmental biology · 2021Review
- CDK Regulation of Meiosis: Lessons fromGenes · 2020Review
- A Transcriptomic Analysis of Saccharomyces cerevisiae Under the Stress of 2-Phenylethanol.Current microbiology · 2018Article
- Diversification of a protein kinase cascade: IME-2 is involved in nonself recognition and programmed cell death in Neurospora crassa.Genetics · 2012Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundIn Saccharomyces cerevisiae, the G1 cyclin/cyclin-dependent kinase (CDK) complexes Cln1,-2,-3/Cdk1 promote S phase entry during the mitotic cell cycle but do not function during meiosis. It has been proposed that the meiosis-specific protein kinase Ime2, which is required for normal timing of pre-meiotic DNA replication, is equivalent to Cln1,-2/Cdk1. These two CDK complexes directly catalyze phosphorylation of the B-type cyclin/CDK inhibitor Sic1 during the cell cycle to enable its destruction. As a result, Clb5,-6/Cdk1 become activated and facilitate initiation of DNA replication. While Ime2 is required for Sic1 destruction during meiosis, evidence now suggests that Ime2 does not directly catalyze Sic1 phosphorylation to target it for destabilization as Cln1,-2/Cdk1 do during the cell cycle. METHODOLOGY/PRINCIPAL
findingsWe demonstrated that Sic1 is eventually degraded in meiotic cells lacking the IME2 gene (ime2Δ), supporting an indirect role of Ime2 in Sic1 destruction. We further examined global RNA expression comparing wild type and ime2Δ cells. Analysis of these expression data has provided evidence that Ime2 is required early in meiosis for normal transcription of many genes that are also periodically expressed during late G1 of the cell cycle. CONCLUSIONS/SIGNIFICANCE: Our results place Ime2 at a position in the early meiotic pathway that lies upstream of the position occupied by Cln1,-2/Cdk1 in the analogous cell cycle pathway. Thus, Ime2 may functionally resemble Cln3/Cdk1 in promoting S phase entry, or it could play a role even further upstream in the corresponding meiotic cascade.
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