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First published online 15 August 2006
doi: 10.1242/jcs.03082
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Research Article |

1 UMR 7622 CNRS, Université Paris 6, 9 Quai St Bernard, Case 24, 75252 Paris cedex 05, France
2 UMR 7009 CNRS, Université Paris 6, Station Zoologique, Observatoire Océanologique, 06234 Villefranche-sur-Mer cedex, France
3 UMR 7628 CNRS, Observatoire Océanologique de Banyuls, Université P. et M. Curie / CNRS / INSU, BP 44, 66651, Banyuls-sur-mer cedex, France
Author for correspondence (e-mail: brigitte.ciapa{at}snv.jussieu.fr)
Accepted 5 June 2006
Unfertilized sea urchin eggs that are arrested at G1 phase after completion of meiosis contain a highly phosphorylated mitogen-activated protein (MAP) kinase (MAPK), the ERK-like protein (ERK-LP). Several data including our previous results show that ERK-LP is inactivated after fertilization, which agrees with results obtained in other species including Xenopus, starfish and mammals. The question is to elucidate the function of a high MAPK activity in sea urchin eggs. We report here that dephosphorylation of ERK-LP with very low concentrations of two MEK inhibitors, PD98059 or U0126, triggers entry into mitosis. Under these conditions, recurrent oscillations of the phosphorylation of ERK-LP and of a tyrosine residue in Cdc2 occur, and the intracellular Ca2+ level (Ca2+i) progressively and slowly increases. Nuclear envelope breakdown and all mitotic events initiated after dephosphorylation of ERK-LP are inhibited when changes in Ca2+i are prevented; however, they are independent of the intracellular pH. These results suggest that inactivation of a MEK-ERK pathway, normally induced after fertilization of sea urchin eggs, triggers entry into mitosis by altering Ca2+i but cannot trigger full DNA replication. We discuss the hypothesis that neither inactivation nor activation of a MEK-ERK pathway is required for S phase completion in sea urchin egg.
Key words: MAP kinase, Egg, Oocyte, Sea urchin, ERK, Mitosis, Calcium, MPF, Fertilization
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