ArticleScientific reports2017
Delayed APC/C activation extends the first mitosis of mouse embryos.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 13 citations in OpenAlex.
- Delays in the final stages of fertilization are strongly associated with trichotomous cytokinesis and cleavage arrest.Journal of assisted reproduction and genetics · 2025Article
- Early onset of APC/C activity renders SAC inefficient in mouse embryos.Frontiers in cell and developmental biology · 2024Article
- Article
- Multiple Roles of PLK1 in Mitosis and Meiosis.Cells · 2023Review
- Mysteries in embryonic development: How can errors arise so frequently at the beginning of mammalian life?PLoS biology · 2019Article
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Authors and funding
4 authors at 4 institutions in 2 countries.
Funding
Abstract
The correct temporal regulation of mitosis underpins genomic stability because it ensures the alignment of chromosomes on the mitotic spindle that is required for their proper segregation to the two daughter cells. Crucially, sister chromatid separation must be delayed until all the chromosomes have attached to the spindle; this is achieved by the Spindle Assembly Checkpoint (SAC) that inhibits the Anaphase Promoting Complex/Cyclosome (APC/C) ubiquitin ligase. In many species the first embryonic M-phase is significantly prolonged compared to the subsequent divisions, but the reason behind this has remained unclear. Here, we show that the first M-phase in the mouse embryo is significantly extended due to a delay in APC/C activation. Unlike in somatic cells, where the APC/C first targets cyclin A2 for degradation at nuclear envelope breakdown (NEBD), we find that in zygotes cyclin A2 remains stable for a significant period of time after NEBD. Our findings that the SAC prevents cyclin A2 degradation, whereas over-expressed Plk1 stimulates it, support our conclusion that the delay in cyclin A2 degradation is caused by low APC/C activity. As a consequence of delayed APC/C activation cyclin B1 stability in the first mitosis is also prolonged, leading to the unusual length of the first M-phase.
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Registered trials
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