<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Lara-Gonzalez P</submitter><funding>ODCDC CDC HHS</funding><funding>National Institutes of Health</funding><funding>NIH Office of Research Infrastructure Programs</funding><funding>Ludwig Institute for Cancer Research</funding><funding>NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>e202308034</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11303871</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>223(11)</volume><pubmed_abstract>Mitosis in early embryos often proceeds at a rapid pace, but how this pace is achieved is not understood. Here, we show that cyclin B3 is the dominant driver of rapid embryonic mitoses in the C. elegans embryo. Cyclins B1 and B2 support slow mitosis (NEBD to anaphase ∼600 s), but the presence of cyclin B3 dominantly drives the approximately threefold faster mitosis observed in wildtype. Multiple mitotic events are slowed down in cyclin B1 and B2-driven mitosis, and cyclin B3-associated Cdk1 H1 kinase activity is ∼25-fold more active than cyclin B1-associated Cdk1. Addition of cyclin B1 to fast cyclin B3-only mitosis introduces an ∼60-s delay between completion of chromosome alignment and anaphase onset; this delay, which is important for segregation fidelity, is dependent on inhibitory pho</pubmed_abstract><journal>The Journal of cell biology</journal><pubmed_title>Cyclin B3 is a dominant fast-acting cyclin that drives rapid early embryonic mitoses.</pubmed_title><pmcid>PMC11303871</pmcid><funding_grant_id>R35 GM150786</funding_grant_id><funding_grant_id>GM147265</funding_grant_id><funding_grant_id>GM074215</funding_grant_id><funding_grant_id>F32GM145068</funding_grant_id><funding_grant_id>P40 OD010440</funding_grant_id><funding_grant_id>S10 OD021724</funding_grant_id><funding_grant_id>R01 GM074215</funding_grant_id><funding_grant_id>R01 GM147265</funding_grant_id><funding_grant_id>GM150786</funding_grant_id><funding_grant_id>F32 GM145068</funding_grant_id><pubmed_authors>Schlientz A</pubmed_authors><pubmed_authors>Variyar S</pubmed_authors><pubmed_authors>Budrewicz J</pubmed_authors><pubmed_authors>Oegema K</pubmed_authors><pubmed_authors>Varshney N</pubmed_authors><pubmed_authors>Bellaart A</pubmed_authors><pubmed_authors>Desai A</pubmed_authors><pubmed_authors>Lara-Gonzalez P</pubmed_authors><pubmed_authors>Nguyen ACN</pubmed_authors><pubmed_authors>Kizhedathu A</pubmed_authors><pubmed_authors>Moghareh S</pubmed_authors><pubmed_authors>Bardwell L</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cyclin B3 is a dominant fast-acting cyclin that drives rapid early embryonic mitoses.</name><description>Mitosis in early embryos often proceeds at a rapid pace, but how this pace is achieved is not understood. Here, we show that cyclin B3 is the dominant driver of rapid embryonic mitoses in the C. elegans embryo. Cyclins B1 and B2 support slow mitosis (NEBD to anaphase ∼600 s), but the presence of cyclin B3 dominantly drives the approximately threefold faster mitosis observed in wildtype. Multiple mitotic events are slowed down in cyclin B1 and B2-driven mitosis, and cyclin B3-associated Cdk1 H1 kinase activity is ∼25-fold more active than cyclin B1-associated Cdk1. Addition of cyclin B1 to fast cyclin B3-only mitosis introduces an ∼60-s delay between completion of chromosome alignment and anaphase onset; this delay, which is important for segregation fidelity, is dependent on inhibitory pho</description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Nov</publication><modification>2026-06-02T10:17:18.899Z</modification><creation>2025-04-19T06:00:24.698Z</creation></dates><accession>S-EPMC11303871</accession><cross_references><pubmed>39105756</pubmed><doi>10.1083/jcb.202308034</doi></cross_references></HashMap>