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A Role for the MEK-MAPK Pathway in Okadaic Acid-Induced Meiotic Resumption of Incompetent Growing Mouse Oocytes1

A Role for the MEK-MAPK Pathway in Okadaic Acid-Induced Meiotic Resumption of Incompetent Growing... AbstractFully grown competent mouse oocytes spontaneously resume meiosis in vitro when released from their follicular environment, in contrast to growing incompetent oocytes, which remain blocked in prophase I. The cell cycle regulators, maturation promoting factor (MPF; [p34cdc2/cyclin B kinase]) and mitogen-activated protein (MAP) kinases (p42MAPK and p44MAPK), are implicated in meiotic competence acquisition. Incompetent oocytes contain levels of p42MAPK, p44MAPK, and cyclin B proteins that are comparable to those in competent oocytes, but their level of p34cdc2 is markedly lower. Okadaic acid (OA), an inhibitor of phosphatases 1 and 2A, induces meiotic resumption of incompetent oocytes. The kinetics and the percentage of germinal vesicle breakdown depends on whether or not oocytes have been cultured before OA treatment. We show that the fast kinetics and the high percentage of germinal vesicle breakdown induced by OA following 2 days in culture is neither the result of an accumulation of p34cdc2 protein, nor to the activation of MPF in incompetent oocytes, but rather by the premature activation of MAP kinases. Indeed, a specific inhibitor of MAPK kinase (MEK) activity, PD98059, inhibits activation of MAP kinases and meiotic resumption. Altogether, these results indicate that the MEK-MAPK pathway is implicated in OA-induced meiotic resumption of incompetent mouse oocytes, and that the MEK-MAPK pathway can induce meiotic resumption in the absence of MPF activation. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Biology of Reproduction Oxford University Press

A Role for the MEK-MAPK Pathway in Okadaic Acid-Induced Meiotic Resumption of Incompetent Growing Mouse Oocytes1

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References (89)

Publisher
Oxford University Press
Copyright
© 2000 by the Society for the Study of Reproduction, Inc.
ISSN
0006-3363
eISSN
1529-7268
DOI
10.1095/biolreprod63.2.658
Publisher site
See Article on Publisher Site

Abstract

AbstractFully grown competent mouse oocytes spontaneously resume meiosis in vitro when released from their follicular environment, in contrast to growing incompetent oocytes, which remain blocked in prophase I. The cell cycle regulators, maturation promoting factor (MPF; [p34cdc2/cyclin B kinase]) and mitogen-activated protein (MAP) kinases (p42MAPK and p44MAPK), are implicated in meiotic competence acquisition. Incompetent oocytes contain levels of p42MAPK, p44MAPK, and cyclin B proteins that are comparable to those in competent oocytes, but their level of p34cdc2 is markedly lower. Okadaic acid (OA), an inhibitor of phosphatases 1 and 2A, induces meiotic resumption of incompetent oocytes. The kinetics and the percentage of germinal vesicle breakdown depends on whether or not oocytes have been cultured before OA treatment. We show that the fast kinetics and the high percentage of germinal vesicle breakdown induced by OA following 2 days in culture is neither the result of an accumulation of p34cdc2 protein, nor to the activation of MPF in incompetent oocytes, but rather by the premature activation of MAP kinases. Indeed, a specific inhibitor of MAPK kinase (MEK) activity, PD98059, inhibits activation of MAP kinases and meiotic resumption. Altogether, these results indicate that the MEK-MAPK pathway is implicated in OA-induced meiotic resumption of incompetent mouse oocytes, and that the MEK-MAPK pathway can induce meiotic resumption in the absence of MPF activation.

Journal

Biology of Reproduction – Oxford University Press

Published: Aug 1, 2000

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