p90Rsk is not involved in cytostatic factor arrest in mouse oocytes.
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 Mos-MAPK 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.
Dumont
Julien
J
Equipe Divisions Méiotiques chez la souris, UMR7622, Centre National de la Recherche Scientifique/Université Pierre et Marie Curie, Paris, France.
Umbhauer
Muriel
M
Rassinier
Pascale
P
Hanauer
André
A
Verlhac
Marie-Hélène
MH
D000818:Animals; D001757:Blastomeres / Q000502:physiology*; D005260:Female; D020935:MAP Kinase Signaling System / Q000235:genetics / Q000502:physiology*; D008540:Meiosis / Q000502:physiology*; D051379:Mice; D018345:Mice, Knockout; D009865:Oocytes / Q000502:physiology*; D011247:Pregnancy; D017231:Proto-Oncogene Proteins c-mos / Q000235:genetics / Q000378:metabolism*; D038744:Ribosomal Protein S6 Kinases, 90-kDa / Q000235:genetics / Q000378:metabolism*; D014982:Xenopus laevis
D017231:Proto-Oncogene Proteins c-mos; D038744:Ribosomal Protein S6 Kinases, 90-kDa