ArticlePloS one2007
Role for non-proteolytic control of M-phase-promoting factor activity at M-phase exit.
Article in PloS one, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 30 citations in OpenAlex.
- Recent advances in understanding the role of Cdk1 in the Spindle Assembly Checkpoint.F1000Research · 2020Review
- LIN-41 inactivation leads to delayed centrosome elimination and abnormal chromosome behavior during female meiosis in Caenorhabditis elegans.Molecular biology of the cell · 2016Article
- The Fcp1-Wee1-Cdk1 axis affects spindle assembly checkpoint robustness and sensitivity to antimicrotubule cancer drugs.Cell death and differentiation · 2015Article
- Kv3.4 potassium channel-mediated electrosignaling controls cell cycle and survival of irradiated leukemia cells.Pflugers Archiv : European journal of physiology · 2013Article
- Cdc25B phosphatase participates in maintaining metaphase II arrest in mouse oocytes.Molecules and cells · 2013Article
- Cdc25A activity is required for the metaphase II arrest in mouse oocytes.Journal of cell science · 2013Article
- The end of mitosis from a phosphatase perspective.Cell cycle (Georgetown, Tex.) · 2013Article
- Intercellular redistribution of cAMP underlies selective suppression of cancer cell growth by connexin26.PloS one · 2013Article
- Carboxy-terminal phosphorylation sites in Cdc25 contribute to enforcement of the DNA damage and replication checkpoints in fission yeast.Current genetics · 2012Article
- Fcp1-dependent dephosphorylation is required for M-phase-promoting factor inactivation at mitosis exit.Nature communications · 2012Article
- Protein tyrosine kinase Wee1B is essential for metaphase II exit in mouse oocytes.Science (New York, N.Y.) · 2011Article
- Human Cdc14B promotes progression through mitosis by dephosphorylating Cdc25 and regulating Cdk1/cyclin B activity.PloS one · 2011Article
- Identification of genes affecting the toxicity of anti-cancer drug bortezomib by genome-wide screening in S. pombe.PloS one · 2011Article
- Canonical and Alternative Pathways in Cyclin-Dependent Kinase 1/Cyclin B Inactivation upon M-Phase Exit in Xenopus laevis Cell-Free Extracts.Enzyme research · 2011Article
- Regulated activity of PP2A-B55 delta is crucial for controlling entry into and exit from mitosis in Xenopus egg extracts.The EMBO journal · 2009Article
- Control of mitotic exit by PP2A regulation of Cdc25C and Cdk1.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
M-phase Promoting Factor (MPF; the cyclin B-cdk 1 complex) is activated at M-phase onset by removal of inhibitory phosphorylation of cdk1 at thr-14 and tyr-15. At M-phase exit, MPF is destroyed by ubiquitin-dependent cyclin proteolysis. Thus, control of MPF activity via inhibitory phosphorylation is believed to be particularly crucial in regulating transition into, rather than out of, M-phase. Using the in vitro cell cycle system derived form Xenopus eggs, here we show, however, that inhibitory phosphorylation of cdk1 contributes to control MPF activity during M-phase exit. By sampling extracts at very short intervals during both meiotic and mitotic exit, we found that cyclin B1-associated cdk1 underwent transient inhibitory phosphorylation at tyr-15 and that cyclin B1-cdk1 activity fell more rapidly than the cyclin B1 content. Inhibitory phosphorylation of MPF correlated with phosphorylation changes of cdc25C, the MPF phosphatase, and physical interaction of cdk1 with wee1, the MPF kinase, during M-phase exit. MPF down-regulation required Ca(++)/calmodulin-dependent kinase II (CaMKII) and cAMP-dependent protein kinase (PKA) activities at meiosis and mitosis exit, respectively. Treatment of M-phase extracts with a mutant cyclin B1-cdk1AF complex, refractory to inhibition by phosphorylation, impaired binding of the Anaphase Promoting Complex/Cyclosome (APC/C) to its co-activator Cdc20 and altered M-phase exit. Thus, timely M-phase exit requires a tight coupling of proteolysis-dependent and proteolysis-independent mechanisms of MPF 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.