Dumont Julien, Umbhauer Muriel, Rassinier Pascale, Hanauer André, Verlhac Marie-Hélène
Equipe Divisions Méiotiques chez la souris, UMR7622, Centre National de la Recherche Scientifique/Université Pierre et Marie Curie, Paris, France.
J Cell Biol. 2005 Apr 25;169(2):227-31. doi: 10.1083/jcb.200501027. Epub 2005 Apr 18.
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.
脊椎动物的卵母细胞停滞在第二次减数分裂中期（MII），由于细胞静止因子（CSF）的活性，它们在该阶段维持高cdc2/细胞周期蛋白B活性以及稳定的双极纺锤体。Mos-MAPK途径对于建立CSF至关重要。实际上，mos-/-品系的卵母细胞不会停滞在MII期，而是会在未受精的情况下激活，这与注射针对Mos的吗啉代寡核苷酸的非洲爪蟾卵母细胞的情况相同。在非洲爪蟾卵母细胞中，MAPK底物p90Rsk（核糖体S6激酶）是CSF活性的主要介导因子。我们在此表明，在小鼠卵母细胞中情况并非如此。注射组成型活性突变形式的Rsk1和Rsk2不会诱导二细胞期小鼠胚胎的细胞周期停滞。此外，将这两种突变形式注射到mos-/-卵母细胞中后，它们也无法恢复MII期停滞。最终，三敲除Rsk（1、2、3）的卵母细胞呈现出正常的CSF停滞。我们证明p90Rsk不参与小鼠卵母细胞的MII期停滞。
