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Chromosome condensation in pig oocytes: Lack of a requirement for either cdc2 kinase or MAP kinase activity
Author(s) -
Kubelka Michal,
Anger Martin,
Kalous Jaroslav,
Schultz Richard M.,
MotlÍk Jan
Publication year - 2002
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.10176
Subject(s) - germinal vesicle , biology , premature chromosome condensation , cyclin dependent kinase 1 , okadaic acid , kinase , cyclin dependent kinase , microbiology and biotechnology , cyclin dependent kinase 2 , maturation promoting factor , cyclin dependent kinase 4 , protein kinase a , phosphatase , biochemistry , oocyte , phosphorylation , cell cycle , embryo , cell
In this study, butyrolactone I (BL I), a potent and specific inhibitor of cyclin‐dependent kinases (cdk), is shown to inhibit germinal vesicle breakdown (GVBD) in pig oocytes. Oocytes treated with 100 μM BL I were arrested in the germinal vesicle (GV)‐stage and displayed low activity of cdc2 kinase and MAP kinase. Nevertheless, chromosome condensation occurred and highly condensed bivalents were seen within an intact GV after a 24‐hr culture in the presence of BL I. The inhibitory effect of BL I on MAP kinase activation during culture was likely mediated through a cdk‐dependent pathway, since MAP kinase activity present in extracts derived from metaphase II eggs was not inhibited by BL I. The block of GVBD could be released by treating oocytes with okadaic acid (OA), an inhibitor of type 1 and 2A phosphatases; 82% of the oocytes treated with the combination of OA/BL I underwent GVBD, and MAP kinase became activated, while cdc2 kinase remained inhibited. These results suggest that both chromosome condensation and GVBD could occur without activation of cdc2 kinase, whereas an increase in MAP kinase activity may be a requisite for GVBD in pig oocytes in conditions when cdc2 kinase activation is blocked by BL I. Mol. Reprod. Dev. 63: 110–118, 2002. © 2002 Wiley‐Liss, Inc.