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Titolo:
Analysis of the mechanism(s) of metaphase I-arrest in strain LT mouse oocytes: Delay in the acquisition of competence to undergo the metaphase I/anaphase transition
Autore:
Hirao, Y; Eppig, JJ;
Indirizzi:
Jackson Lab, Bar Harbor, ME 04609 USA Jackson Lab Bar Harbor ME USA 04609Jackson Lab, Bar Harbor, ME 04609 USA
Titolo Testata:
MOLECULAR REPRODUCTION AND DEVELOPMENT
fascicolo: 3, volume: 54, anno: 1999,
pagine: 311 - 318
SICI:
1040-452X(199911)54:3<311:AOTMOM>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
MATURATION-PROMOTING FACTOR; CELL-CYCLE; PARTHENOGENETIC DEVELOPMENT; MEIOTIC METAPHASE; TOPOISOMERASE-II; KINASE-ACTIVITY; LT/SV MICE; MEIOSIS-I; MOS; ACTIVATION;
Keywords:
mouse; oocytes; meiosis; metaphase I-arrest; cytostatic factor; MOS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Eppig, JJ Jackson Lab, 600 Main St, Bar Harbor, ME 04609 USA Jackson Lab 600 Main St Bar Harbor ME USA 04609 or, ME 04609 USA
Citazione:
Y. Hirao e J.J. Eppig, "Analysis of the mechanism(s) of metaphase I-arrest in strain LT mouse oocytes: Delay in the acquisition of competence to undergo the metaphase I/anaphase transition", MOL REPROD, 54(3), 1999, pp. 311-318

Abstract

Fully grown oocytes of most laboratory mice progress without interruption from the germinal vesicle (GV) stage to metaphase ii, where meiosis is arrested until fertilization. In contrast, many oocytes of strain LT mice arrest precociously at metaphase I and often undergo subsequent spontaneous parthenogenetic activation. Cytostatic factor (CSF), which prevents the degradation of cyclin B and maintains high maturation-promoting factor (MPF) activity, is required for maintenance of metaphase I-arrest in LT oocytes, similar to its requirement for maintaining metaphase Ii-arrest in normal oocytes. However, CSF does not instigate metaphase I-arrest since a temporary metaphase I-arrest occurs in MOS-null LT oocytes. This paper addresses the mechanism(s) that may instigate metaphase I-arrest and tests the hypothesis that there may be one or more defects in LT oocytes that delay their acquisition of competence to trigger the cascade of processes that normally drive entry into and progression through anaphase I. To test this hypothesis, MPF activity was artificially abrogated by treating oocytes with a general protein kinase inhibitor, 6-DMAP, at various times during the progression of meiosis I. This allowed a comparison of the time at which LT and normal oocytes become competent to undergo the metaphase I/anaphase transition even if oocytes were arrested at metaphase I when 6-DMAP-treatment was begun. There were no differences between LT and control oocytes in the kinetics of MPF suppression by 6-DMAP. However, it was found that LT oocytes do not acquire competence to undergo the metaphase I/anaphase transition in response to 6-DMAP until 50-60 min after normal oocytes. A similar delay was observed in strain CX8-4 oocytes, which also have a high incidence of metaphase I-arrest, but not in strain CX8-11 oocytes, which exhibit a low incidence of metaphase I-arrest. MOS-null LT oocytes also exhibit a delay in acquisition of competence to undergo the metaphase I/anaphase transition. Thus, a delay in competence to undergo the metaphase I/anaphase transition in response to 6-DMAP-treatment correlates with metaphase I-arrest. It is therefore hypothesized that the observed delay in acquisition of competence to enter anaphaseI may instigate the sustained metaphase I-arrest in LT oocytes by allowingCSF activity to rise to a level that prevents cyclin B degradation and maintains high MPF activity before anaphase can be initiated by normal triggering mechanisms. (C) 1999 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 04:47:15