ArticleCell cycle (Georgetown, Tex.)2014
Regulation of wee1(+) expression during meiosis in fission yeast.
Article in Cell cycle (Georgetown, Tex.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Wee Kinases, Big Impact: Wee and Myt Kinases as Critical Regulators of Meiotic Progression.Journal of developmental biology · 2026Review
- Sporulation: A response to starvation in the fission yeast Schizosaccharomyces pombe.MicrobiologyOpen · 2022Review
- TheBiomolecules · 2021Article
- Modeling the Control of Meiotic Cell Divisions: Entry, Progression, and Exit.Biophysical journal · 2020Article
- CDK Regulation of Meiosis: Lessons fromGenes · 2020Review
- Targeting condensin, a vital spot of MYCN-amplified neuroblastoma.Cell cycle (Georgetown, Tex.) · 2014Article
- Dangerous liaisons: MYCN meets condensins.Cell cycle (Georgetown, Tex.) · 2014Article
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Authors and funding
4 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In eukaryotes, the cyclin-dependent kinase Cdk1p (Cdc2p) plays a central role in entry into and progression through nuclear division during mitosis and meiosis. Cdk1p is activated during meiotic nuclear divisions by dephosphorylation of its tyrosine-15 residue. The phosphorylation status of this residue is largely determined by the Wee1p kinase and the Cdc25p phosphatase. In fission yeast, the forkhead-type transcription factor Mei4p is essential for entry into the first meiotic nuclear division. We recently identified cdc25(+) as an essential target of Mei4p in the control of entry into meiosis I. Here, we show that wee1(+) is another important target of Mei4p in the control of entry into meiosis I. Mei4p bound to the upstream region of wee1(+) in vivo and in vitro and inhibited expression of wee1(+), whereas Mei4p positively regulated expression of the adjacent pseudogene. Overexpression of Mei4p inhibited expression of wee1(+) and induced that of the pseudogene. Conversely, deletion of Mei4p did not decrease expression of wee1(+) but inhibited that of the pseudogene. In addition, deletion of Mei4p-binding regions delayed repression of wee1(+) expression as well as induction of expression of the pseudogene. These results suggest that repression of wee1(+) expression is primarily owing to Mei4p-mediated transcriptional interference.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.