ArticleMolecular biology of the cell2009
Mitotic exit in the absence of separase activity.
Article in Molecular biology of the cell, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 35 citations in OpenAlex.
- The AMPK kinase Sak1 activates separase and promotes its nuclear localization during mitosis.The Journal of cell biology · 2026Article
- Modeling the START transition in the budding yeast cell cycle.PLoS computational biology · 2024Article
- Characterization of a novel separase-interacting protein and candidate new securin, Eip1p, in the fungal pathogenMolecular biology of the cell · 2019Article
- Article
- Genetic instability in budding and fission yeast-sources and mechanisms.FEMS microbiology reviews · 2015Review
- A role for the budding yeast separase, Esp1, in Ty1 element retrotransposition.PLoS genetics · 2015Article
- Cdc14 Early Anaphase Release, FEAR, Is Limited to the Nucleus and Dispensable for Efficient Mitotic Exit.PloS one · 2015Article
- From START to FINISH: computational analysis of cell cycle control in budding yeast.NPJ systems biology and applications · 2015Article
- Licensing of yeast centrosome duplication requires phosphoregulation of sfi1.PLoS genetics · 2014Article
- Article
- The Mitotic Exit Network and Cdc14 phosphatase initiate cytokinesis by counteracting CDK phosphorylations and blocking polarised growth.The EMBO journal · 2012Article
- Zds1 regulates PP2A(Cdc55) activity and Cdc14 activation during mitotic exit through its Zds_C motif.Journal of cell science · 2012Article
- Article
- Dependence of Chs2 ER export on dephosphorylation by cytoplasmic Cdc14 ensures that septum formation follows mitosis.Molecular biology of the cell · 2012Article
- Computational modelling of mitotic exit in budding yeast: the role of separase and Cdc14 endocycles.Journal of the Royal Society, Interface · 2011Article
- Phosphatases: providing safe passage through mitotic exit.Nature reviews. Molecular cell biology · 2011Review
- Global analysis of Cdc14 phosphatase reveals diverse roles in mitotic processes.The Journal of biological chemistry · 2011Article
- Efficient and rapid exact gene replacement without selection.Yeast (Chichester, England) · 2011Article
- Oscillatory dynamics of cell cycle proteins in single yeast cells analyzed by imaging cytometry.PloS one · 2011Article
- One-hit wonders of genomic instability.Cell division · 2010Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In budding yeast, three interdigitated pathways regulate mitotic exit (ME): mitotic cyclin-cyclin-dependent kinase (Cdk) inactivation; the Cdc14 early anaphase release (FEAR) network, including a nonproteolytic function of separase (Esp1); and the mitotic exit network (MEN) driven by interaction between the spindle pole body and the bud cortex. Here, we evaluate the contributions of these pathways to ME kinetics. Reducing Cdk activity is critical for ME, and the MEN contributes strongly to ME efficiency. Esp1 contributes to ME kinetics mainly through cohesin cleavage: the Esp1 requirement can be largely bypassed if cells are provided Esp1-independent means of separating sister chromatids. In the absence of Esp1 activity, we observed only a minor ME delay consistent with a FEAR defect. Esp1 overexpression drives ME in Cdc20-depleted cells arrested in metaphase. We have found that this activity of overexpressed Esp1 depended on spindle integrity and the MEN. We defined the first quantitative measure for Cdc14 release based on colocalization with the Net1 nucleolar anchor. This measure indicates efficient Cdc14 release upon MEN activation; release driven by Esp1 in the absence of microtubules was inefficient and incapable of driving ME. We also found a novel role for the MEN: activating Cdc14 nuclear export, even in the absence of Net1.
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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.