Induction of precocious germinal vesicle breakdown (GVB) by GVB-incompetent mouse oocytes: possible role of mitogen-activated protein kinases rather than p34cdc2 kinase.
Biol Reprod
; 52(4): 895-902, 1995 Apr.
Article
en En
| MEDLINE
| ID: mdl-7780012
ABSTRACT
In contrast to fully grown mouse oocytes, growing oocytes released from their preantral follicles are not capable of resuming meiosis spontaneously. However, when these denuded growing oocytes are incubated for 2-3 days in control medium and then treated with okadaic acid, 95% undergo precocious germinal vesicle breakdown (GVB) and chromosome condensation within 24 h. This study shows that both events apparently occur through a p34cdc2 kinase-independent pathway, since activity of this kinase was detected only after the oocytes had undergone okadaic acid-stimulated GVB. In contrast, microtubule-associated or mitogen-activated protein (MAP) kinases 1 and 2 were activated before GVB and their level of activity was correlated with the percentage of oocytes undergoing GVB, suggesting that these kinases may promote GVB and chromosome condensation under these experimental conditions. In addition, it is shown that MAP kinases accumulate during normal oocyte growth in vivo, but not in cultured denuded oocytes in vitro even when these oocytes become competent to undergo okadaic acid-stimulated GVB. Unlike p34cdc2, the accumulation of MAP kinases requires close physical interactions between the oocytes and the granulosa cells but is not necessary for the oocyte to become GVB-competent. Therefore, it MAP kinases are actually involved in the induction of GVB and chromosome condensation during normal oocyte maturation, acquisition of GVB competence requires oocyte-autonomous accumulation of MAP kinase activator(s) rather than the MAP kinases themselves.
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Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Oocitos
/
Proteína Quinasa CDC2
/
Proteínas Quinasas Dependientes de Calcio-Calmodulina
Límite:
Animals
Idioma:
En
Revista:
Biol Reprod
Año:
1995
Tipo del documento:
Article
País de afiliación:
Estados Unidos