Published online 18 April 2005. doi:10.1083/jcb.200501027
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 169, Number 2, 227-231
p90Rsk is not involved in cytostatic factor arrest in mouse oocytes
Julien Dumont1,
Muriel Umbhauer2,
Pascale Rassinier1,
André Hanauer3, and
Marie-Hélène Verlhac1
1 Equipe Divisions Méiotiques chez la souris, UMR7622, Centre National de la Recherche Scientifique/Université Pierre et Marie Curie, 75252, Paris, cedex 05, France
2 Equipe Signalisation et Morphogénèse, UMR7622, Centre National de la Recherche Scientifique/Université Pierre et Marie Curie, 75252, Paris, cedex 05, France
3 Institut de Génétique et de Biologie Moléculaire et Cellulaire, BP10142, 67404 Illkrich cedex, Strasbourg, France
Correspondence to Marie-Hélène Verlhac: Marie-Helene.Verlhac{at}snv.jussieu.fr
Abstract
Vertebrate oocytes arrest in metaphase of the second meiotic division (MII), where they maintain a high cdc2/cyclin B activity and a stable, bipolar spindle because of cytostatic factor (CSF) activity. The MosMAPK pathway is essential for establishing CSF. Indeed, oocytes from the mos/ strain do not arrest in MII and activate without fertilization, as do Xenopus laevis oocytes injected with morpholino oligonucleotides directed against Mos. In Xenopus oocytes, p90Rsk (ribosomal S6 kinase), a MAPK substrate, is the main mediator of CSF activity. We show here that this is not the case in mouse oocytes. The injection of constitutively active mutant forms of Rsk1 and Rsk2 does not induce a cell cycle arrest in two-cell mouse embryos. Moreover, these two mutant forms do not restore MII arrest after their injection into mos/ oocytes. Eventually, oocytes from the triple Rsk (1, 2, 3) knockout present a normal CSF arrest. We demonstrate that p90Rsk is not involved in the MII arrest of mouse oocytes.
Abbreviations used in this paper: CSF, cytostatic factor; ERK, extracellular regulated kinase; GVBD, germinal vesicle breakdown; MEK, MAPK/ERK kinase; MII, metaphase of the second meiotic division.

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