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Germinal vesicle breakdown is not fully dependent on MAPK activation in maturing oocytes of marine nemertean worms
Author(s) -
Smythe T.L.,
Stricker S.A.
Publication year - 2005
Publication title -
molecular reproduction and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.745
H-Index - 105
eISSN - 1098-2795
pISSN - 1040-452X
DOI - 10.1002/mrd.20188
Subject(s) - germinal vesicle , biology , mapk/erk pathway , cyclin dependent kinase 1 , kinase , maturation promoting factor , microbiology and biotechnology , protein kinase a , cyclin b , phosphorylation , cyclin , oocyte , cell cycle , biochemistry , cell , embryo
Abstract Previously, it has been shown that oocytes of marine nemertean worms resume meiosis and undergo germinal vesicle breakdown (GVBD) following treatment with either natural seawater (NSW), or the neurohormone serotonin (5‐hydroxytryptamine or 5‐HT). In this investigation of the nemerteans Cerebratulus lacteus and Cerebratulus sp., immunoblots and kinase assays were used to compare the roles of two regulatory kinases: mitogen‐activated protein kinase (MAPK) and Cdc2/cyclin B (referred to as maturation promoting factor or MPF). Based on such analyses, an ERK (extracellular signal regulated kinase) type of MAPK was found to be activated concurrently with Cdc2/cyclin B during NSW‐ and 5‐HT‐induced maturation. MAPK activation occurred prior to GVBD and seemed to be controlled primarily by phosphorylation rather than de novo protein synthesis. Inhibition of MAPK signaling by U0126 was capable of delaying but not permanently blocking Cdc2/cyclin B activation and GVBD in 5‐HT treated oocytes and subsets of NSW‐treated oocytes. Collectively such data indicated that GVBD is not fully dependent on MAPK activation, since Cdc2/cyclin B can apparently be activated by MAPK‐independent mechanism(s) in maturing nemertean oocytes. Mol. Reprod. Dev. 70: 91–102, 2004. © 2004 Wiley‐Liss, Inc.