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Cyclin B1 is essential for mitosis in mouse embryos, and its nuclear export sets the time for mitosis.

Published version
Peer-reviewed

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Authors

Strauss, Bernhard 
Coelho, Paula Almeida  ORCID logo  https://orcid.org/0000-0003-0614-7575
Zernicka-Goetz, Magdalena 

Abstract

There is remarkable redundancy between the Cyclin-Cdk complexes that comprise the cell cycle machinery. None of the mammalian A-, D-, or E-type cyclins are required in development until implantation, and only Cdk1 is essential for early cell divisions. Cyclin B1 is essential for development, but whether it is required for cell division is contentious. Here, we used a novel imaging approach to analyze Cyclin B1-null embryos from fertilization onward. We show that Cyclin B1-/- embryos arrest in G2 phase after just two divisions. This is the earliest arrest of any Cyclin known and places Cyclin B1 with cdk1 as the essential regulators of the cell cycle. We reintroduced mutant proteins into this genetically null background to determine why Cyclin B1 is constantly exported from the nucleus. We found that Cyclin B1 must be exported from the nucleus for the cell to prevent premature entry to mitosis, and retaining Cyclin B1-Cdk1 at the plasma membrane precludes entry to mitosis.

Description

Keywords

Active Transport, Cell Nucleus, Animals, CDC2 Protein Kinase, Cell Cycle Proteins, Cyclin B1, DNA-Binding Proteins, Embryonic Development, Mice, Mice, Knockout, Mitosis, Nuclear Proteins, Phosphorylation, Protein-Tyrosine Kinases, Transcription Factors, cdc25 Phosphatases

Journal Title

J Cell Biol

Conference Name

Journal ISSN

0021-9525
1540-8140

Volume Title

217

Publisher

Rockefeller University Press
Sponsorship
Medical Research Council (G0701184)
Medical Research Council (G1000818)
Isaac Newton Trust (MINUTE 726(K))
Wellcome Trust (092096/Z/10/Z)
Cancer Research Uk (None)