ArticleThe EMBO journal2004
Fission yeast Clp1p phosphatase affects G2/M transition and mitotic exit through Cdc25p inactivation.
Article in The EMBO journal, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 93 citations in OpenAlex.
- The mitotic functions of a fission yeast CK1 enzyme are regulated by Cdk1-dependent and auto-phosphorylation.The Journal of biological chemistry · 2026Article
- The Cdc14 phosphatase, Clp1, does not affect genome expression.microPublication biology · 2024Article
- Fission yeast Cdc14-like phosphatase Flp1/Clp1 modulates the transcriptional response to oxidative stress.Scientific reports · 2023Article
- The diverging role of CDC14B: from mitotic exit in yeast to cell fate control in humans.The EMBO journal · 2023Review
- Ubiquitination of CLIP-170 family protein restrains polarized growth upon DNA replication stress.Nature communications · 2022Article
- Article
- TORC1 inactivation promotes APC/C-dependent mitotic slippage in yeast and human cells.iScience · 2022Article
- Uncoupling of Mitosis and Cytokinesis Upon a Prolonged Arrest in Metaphase Is Influenced by Protein Phosphatases and Mitotic Transcription in Fission Yeast.Frontiers in cell and developmental biology · 2022Article
- Review
- Caffeine as a tool for investigating the integration of Cdc25 phosphorylation, activity and ubiquitin-dependent degradation inCell division · 2020Review
- Biochemical analyses reveal amino acid residues critical for cell cycle-dependent phosphorylation of human Cdc14A phosphatase by cyclin-dependent kinase 1.Scientific reports · 2018Article
- Characterization of aBiology open · 2018Article
- MoCDC14 is important for septation during conidiation and appressorium formation in Magnaporthe oryzae.Molecular plant pathology · 2018Article
- Dialogue between centrosomal entrance and exit scaffold pathways regulates mitotic commitment.The Journal of cell biology · 2017Article
- Size-Dependent Expression of the Mitotic Activator Cdc25 Suggests a Mechanism of Size Control in Fission Yeast.Current biology : CB · 2017Article
- Wee1 and Cdc25: Tools, pathways, mechanisms, questions.Cell cycle (Georgetown, Tex.) · 2017Article
- Wee1 and Cdc25 are controlled by conserved PP2A-dependent mechanisms in fission yeast.Cell cycle (Georgetown, Tex.) · 2017Article
- Identification of a Sgo2-Dependent but Mad2-Independent Pathway Controlling Anaphase Onset in Fission Yeast.Cell reports · 2017Article
- MST kinases in development and disease.The Journal of cell biology · 2015Review
- Characterization of the roles of Blt1p in fission yeast cytokinesis.Molecular biology of the cell · 2014Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The Cdc14 family of phosphatases specifically reverses proline-directed phosphorylation events. In Saccharomyces cerevisiae, Cdc14p promotes Cdk1p inactivation at mitotic exit by reversing Cdk1p-dependent phosphorylations. Cdk1p is a proline-directed kinase whose activity is required in all eukaryotes for the transit into mitosis. At mitotic commitment, Cdk1p participates in its own regulation by activating the mitotic inducing phosphatase, Cdc25p, and inhibiting the opposing kinase, Wee1p. We have investigated the ability of Schizosaccharomyces pombe Clp1p, a Cdc14p homolog, to disrupt this auto-amplification loop. We show here that Clp1p is required to dephosphorylate, destabilize, and inactivate Cdc25p at the end of mitosis. Clp1p promotes recognition of Cdc25p by the anaphase-promoting complex/cyclosome, an E3 ubiquitin ligase. Failure to inactivate and destabilize Cdc25p in late mitosis delays progression through anaphase, interferes with septation initiation network signaling, and additionally advances the commitment to mitotic entry in the next cycle. This may be a widely conserved mechanism whereby Cdc14 proteins contribute to Cdk1p inactivation.
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Registered trials
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.