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Protein phosphorylation in meiotically competent and incompetent mouse oocytes
Author(s) -
Bornslaeger Elayne A.,
Mattei Peter M.,
Schultz Richard M.
Publication year - 1988
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.1080010105
Subject(s) - germinal vesicle , biology , dephosphorylation , phosphoprotein , meiosis , microinjection , oocyte , protein kinase a , phosphorylation , kinase , microbiology and biotechnology , protein phosphorylation , phosphatase , biochemistry , embryo , gene
Specific changes in the two dimensional gel electrophoretic pattern of mouse oocyte phosphoproteins precede germinal vesicle breakdown (GVBD). We report that changes in the relative abundance of phosphoamino acids occurred prior to GVBD. We also report data that further strengthen the close association of the changes in phosphoprotein patterns with resumption of meiosis. The calmodulin antagonist W7, which transiently inhibits GVBD, inhibited partially at least two of the maturation‐associated phosphoprotein changes, the dephosphorylation of a 60,000 M r 24,000 and 28,000 occurred; all these changes occurred, however, in oocytes from juvenile mice that were competent to resume meiosis. The microinjection of the heat‐stable inhibitor of cyclic adenosine monophosphate (cAMP)‐dependent protein kinase (PKI), which induces GVBD in fully grown oocytes, did not induce GVBD in meiotically incompetent oocytes. Microinjected PKI did not induce the increased protein phosphorylations associated with maturation, but it did induce the dephosphorylation of the 60,000 M r phosphoprotein. These results provide molecular markers for commitment to resume meiosis in GV‐intact oocytes and indicate a potential basis for meiotic incompetence.