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Okadaic acid and p13 suc1 modulate the reinitiation of meiosis in mouse oocytes
Author(s) -
Gavin AnneClaude,
Vassalli JeanDominique,
Cavadore JeanClaude,
SchorderetSlatkine Sabine
Publication year - 1992
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.1080330309
Subject(s) - okadaic acid , biology , germinal vesicle , maturation promoting factor , microinjection , oocyte , phosphatase , microbiology and biotechnology , activator (genetics) , phosphorylation , cyclin dependent kinase 1 , meiosis , biochemistry , gene , cell cycle , embryo
Short‐term exposure to okadaic acid (OA), a specific inhibitor of protein phosphatases 1 and 2A, induced resumpton of meiosis, including metaphase spindle formation, in mouse oocytes treated with a phosphodiesterase inhibitor, while long incubations with OA arrested oocyte maturation at a step prior to spindle formation. To explore the basis for this difference, the overall patterns of protein synthesis and phosphorylation and the production of tissue‐type plasminogen activator (tPA), the synthesis of which is induced after germinal vesicle breakdown (GVBD), were analyzed under various OA treatments. Short‐term exposure to OA led to tPA production and did not greatly affect the maturation‐associated changes in protein phosphorylation. By contrast, a long application of OA did not result in tPA production and induced more marked changes in protein phosphorylation. Microinjection into prophase oocytes of the the product of the fission yeast gene p13 suc1 , known to inhibit p34 cdc2 kinase activation and/or activity, prevented meiotic reinitiation. This effect was overcome by microinjection of OA, at concentrations higher than those required for induction of maturation in the absence of p13 suc1 . These observations suggest that inhibition of phosphatase 1 or 2A or both triggers meiotic resumption by acting at the same site or at a site proximal to the p13 suc1 ‐sensitive step of cdc2 kinase activation. © 1992 Wiley‐Liss, Inc.