Toggle Main Menu Toggle Search

ePrints

Securin and not CDK1/cyclin B1 regulates sister chromatid disjunction during meiosis II in mouse eggs

Lookup NU author(s): Ibtissem Nabti, Dr Alexandra Reis, Dr Mark Levasseur, Professor Keith Jones

Downloads

Full text for this publication is not currently held within this repository. Alternative links are provided below where available.


Abstract

Mammalian eggs remain arrested at metaphase of the second meiotic division (metII) for an indeterminate time before fertilization. During this period, which can last several hours, the continued attachment of sister chromatids is thought to be achieved by inhibition of the protease separase. Separase is known to be inhibited by binding either securin or Maturation (M-Phase)-Promoting Factor, a heterodimer of CDK1/cyclin B1. However, the relative contribution of securin and CDK/cyclin B1 to sister chromatid attachment during metII arrest has not been assessed. Although there are conditions in which either CDK1/cyclinB1 activity or securin can prevent sister chromatid disjunction, principally by overexpression of non-degradable cyclin B1 or securin, we find here that separase activity is primarily regulated by securin and not CDK1/cyclin B1. Thus the CDK1 inhibitor roscovitine and an antibody we designed to block the interaction of CDK1/cyclin B1 with separase, both failed to induce sister disjunction. In contrast, securin morpholino knockdown specifically induced loss of sister attachment, that could be restored by securin cRNA rescue. During metII arrest separase appears primarily regulated by securin binding, not CDK1/cyclin B1. © 2008 Elsevier Inc. All rights reserved.


Publication metadata

Author(s): Nabti I, Reis A, Levasseur M, Stemmann O, Jones KT

Publication type: Article

Publication status: Published

Journal: Developmental Biology

Year: 2008

Volume: 321

Issue: 2

Pages: 379-386

ISSN (print): 0012-1606

ISSN (electronic): 1095-564X

Publisher: Academic Press

URL: http://dx.doi.org/10.1016/j.ydbio.2008.06.036

DOI: 10.1016/j.ydbio.2008.06.036


Altmetrics

Altmetrics provided by Altmetric


Actions

    Link to this publication


Share