ArticleThe Journal of cell biology2008
Separase cooperates with Zds1 and Zds2 to activate Cdc14 phosphatase in early anaphase.
Article in The Journal of cell biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
What it found
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Who cites it
42 citing papers in PubMed, 64 citations in OpenAlex.
- The AMPK kinase Sak1 activates separase and promotes its nuclear localization during mitosis.The Journal of cell biology · 2026Article
- The diverging role of CDC14B: from mitotic exit in yeast to cell fate control in humans.The EMBO journal · 2023Review
- Article
- SUMOylation stabilizes sister kinetochore biorientation to allow timely anaphase.The Journal of cell biology · 2021Article
- The regulation of Net1/Cdc14 by the Hog1 MAPK upon osmostress unravels a new mechanism regulating mitosis.Cell cycle (Georgetown, Tex.) · 2020Review
- The Multiple Roles of the Cdc14 Phosphatase in Cell Cycle Control.International journal of molecular sciences · 2020Review
- PP2A Functions during Mitosis and Cytokinesis in Yeasts.International journal of molecular sciences · 2019Review
- Cdc14 activation requires coordinated Cdk1-dependent phosphorylation of Net1 and PP2A-Cdc55 at anaphase onset.Cellular and molecular life sciences : CMLS · 2019Article
- Ser/Thr protein phosphatases in fungi: structure, regulation and function.Microbial cell (Graz, Austria) · 2019Review
- Characterization of aBiology open · 2018Article
- SILAC-based phosphoproteomics reveals new PP2A-Cdc55-regulated processes in budding yeast.GigaScience · 2018Article
- Protein Kinase C Controls Binding of Igo/ENSA Proteins to Protein Phosphatase 2A in Budding Yeast.The Journal of biological chemistry · 2017Article
- Cdc14 Early Anaphase Release, FEAR, Is Limited to the Nucleus and Dispensable for Efficient Mitotic Exit.PloS one · 2015Article
- Nur1 dephosphorylation confers positive feedback to mitotic exit phosphatase activation in budding yeast.PLoS genetics · 2015Article
- Chromosome segregation in budding yeast: sister chromatid cohesion and related mechanisms.Genetics · 2014Review
- Comparative genetic analysis of PP2A-Cdc55 regulators in budding yeast.Cell cycle (Georgetown, Tex.) · 2014Article
- Cell cycle checkpoint regulators reach a zillion.Cell cycle (Georgetown, Tex.) · 2013Review
- Yeast protein phosphatase 2A-Cdc55 regulates the transcriptional response to hyperosmolarity stress by regulating Msn2 and Msn4 chromatin recruitment.Molecular and cellular biology · 2013Article
- CDK-dependent nuclear localization of B-cyclin Clb1 promotes FEAR activation during meiosis I in budding yeast.PloS one · 2013Article
- Dual Regulation of the mitotic exit network (MEN) by PP2A-Cdc55 phosphatase.PLoS genetics · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Completion of mitotic exit and cytokinesis requires the inactivation of mitotic cyclin-dependent kinase (Cdk) activity. A key enzyme that counteracts Cdk during budding yeast mitotic exit is the Cdc14 phosphatase. Cdc14 is inactive for much of the cell cycle, sequestered by its inhibitor Net1 in the nucleolus. At anaphase onset, separase-dependent down-regulation of PP2A(Cdc55) allows phosphorylation of Net1 and consequent Cdc14 release. How separase causes PP2A(Cdc55) down-regulation is not known. Here, we show that two Cdc55-interacting proteins, Zds1 and Zds2, contribute to timely Cdc14 activation during mitotic exit. Zds1 and Zds2 are required downstream of separase to facilitate nucleolar Cdc14 release. Ectopic Zds1 expression in turn is sufficient to down-regulate PP2A(Cdc55) and promote Net1 phosphorylation. These findings identify Zds1 and Zds2 as new components of the mitotic exit machinery, involved in activation of the Cdc14 phosphatase at anaphase onset. Our results suggest that these proteins may act as separase-regulated PP2A(Cdc55) inhibitors.
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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.