ArticleProceedings of the National Academy of Sciences of the United States of America2004
Emi1-mediated M-phase arrest in Xenopus eggs is distinct from cytostatic factor arrest.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed.
- Contributions of UBE2C and UBE2S to meiotic progression of porcine oocytes.The Journal of reproduction and development · 2018Article
- Transmembrane signal transduction in oocyte maturation and fertilization: focusing on Xenopus laevis as a model animal.International journal of molecular sciences · 2014Review
- Modulation of cell cycle control during oocyte-to-embryo transitions.The EMBO journal · 2013Review
- Translational regulation of the cell cycle: when, where, how and why?Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2011Review
- State of the APC/C: organization, function, and structure.Critical reviews in biochemistry and molecular biology · 2011Review
- Emi2 inhibition of the anaphase-promoting complex/cyclosome absolutely requires Emi2 binding via the C-terminal RL tail.Molecular biology of the cell · 2010Article
- Regulation of APC/C activators in mitosis and meiosis.Annual review of cell and developmental biology · 2008Review
- New insight into metaphase arrest by cytostatic factor: from establishment to release.Oncogene · 2007Review
- A role for Cdc2- and PP2A-mediated regulation of Emi2 in the maintenance of CSF arrest.Current biology : CB · 2007Article
- How eggs arrest at metaphase II: MPF stabilisation plus APC/C inhibition equals Cytostatic Factor.Cell division · 2007Article
- Prophase I arrest and progression to metaphase I in mouse oocytes are controlled by Emi1-dependent regulation of APC(Cdh1).The Journal of cell biology · 2007Article
- The CRY box: a second APCcdh1-dependent degron in mammalian cdc20.EMBO reports · 2006Article
- Mammalian Emi2 mediates cytostatic arrest and transduces the signal for meiotic exit via Cdc20.The EMBO journal · 2006Article
- CaMKII and polo-like kinase 1 sequentially phosphorylate the cytostatic factor Emi2/XErp1 to trigger its destruction and meiotic exit.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Exploring meiotic division in Cargèse. Meeting on meiotic divisions and checkpoints.EMBO reports · 2005Review
- A role for the anaphase-promoting complex inhibitor Emi2/XErp1, a homolog of early mitotic inhibitor 1, in cytostatic factor arrest of Xenopus eggs.Proceedings of the National Academy of Sciences of the United States of America · 2005Article
- Xenopus polo-like kinase Plx1 regulates XErp1, a novel inhibitor of APC/C activity.Genes & development · 2005Article
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oocytes of most vertebrates arrest at metaphase of the second meiosis (meta-II) to await fertilization, thus preventing parthenogenetic activation. This arrest is caused by a cytoplasmic activity called cytostatic factor (CSF), which was first identified in the frog Rana pipiens oocyte >30 years ago. CSF arrest is executed by maintaining the activity of cyclin B-Cdc2 at elevated levels largely through prevention of cyclin B destruction. Although CSF arrest is established by the Mos-mitogen-activated protein kinase pathway and is released by the Ca-calmodulin kinase II pathway, it remains unclear precisely how cyclin B destruction is regulated. Recently, an early mitotic inhibitor, Emi1, was reported to be a critical component of CSF. This report has been expected to provide a final resolution to the CSF problem because Emi1 inhibits the anaphase-promoting complex/cyclosome, a ubiquitin ligase for cyclin B destruction, through sequestration of Cdc20, an activator for the anaphase-promoting complex/cyclosome. In mitotic cycles, however, Emi1 is destroyed in every pro-metaphase, and accordingly, it is unclear why Emi1 should be required for CSF activity, which is seen only in meta-II. Here, we show that Emi1 is absent in unfertilized mature Xenopus eggs and that exogenous Emi1 is destroyed in meta-II and mitotic metaphase. The expression of Emi1 in oocytes hinders meiotic progression. Although both Emi1 and Mos can inhibit progression through M phase, the Emi1-mediated arrest does not require mitogen-activated protein kinase activity and is not released by Ca. Together, our results indicate that Emi1 is unlikely to be a component of CSF.
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