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Titolo:
Evidence that protein kinase C (PKC) participates in the meiosis I to meiosis II transition in mouse oocytes
Autore:
Viveiros, MM; 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:
DEVELOPMENTAL BIOLOGY
fascicolo: 2, volume: 235, anno: 2001,
pagine: 330 - 342
SICI:
0012-1606(20010715)235:2<330:ETPKC(>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
CORTICAL GRANULE EXOCYTOSIS; CELL-CYCLE CONTROL; LT/SV STRAIN MICE; MEIOTIC MATURATION; PARTHENOGENETIC DEVELOPMENT; SECONDARY OOCYTES; EGG ACTIVATION; M-PHASE; ARREST; MOS;
Keywords:
meiosis; anaphase I; protein kinase C; MPF; spontaneous activation; PKC-delta; MAPK;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
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:
M.M. Viveiros et al., "Evidence that protein kinase C (PKC) participates in the meiosis I to meiosis II transition in mouse oocytes", DEVELOP BIO, 235(2), 2001, pp. 330-342

Abstract

Oocytes from LTXBO mice exhibit a delayed entry into anaphase I and frequently enter interphase after the first meiotic division. This unique oocyte model was used to test the hypothesis that protein kinase C (PKC) may regulate the meiosis I-to-meiosis II transition. PKC activity was detected in LTXBO oocytes at prophase I and increased with meiotic maturation, with the highest (P < 0.05) activity observed at late metaphase I(MI). Treatment of late MI-stage oocytes with the PKC inhibitor, bisindolylmaleimide I(BIM), transiently reduced (P < 0.05) M-phase-promoting factor (MPF) activity and promoted (P < 0.05) progression to metaphase II (MII), while mitogen-activated protein kinase (MAPK) activity remained elevated during the MI-to-MII transition. Confocal microscopy analysis of LTXBO oocytes during this transition showed PKC-delta associated with the meiotic spindle and then with the chromosomes at MII. Inhibition of PKC activity also prevented untimely entryinto interphase, but only when PKC activity was reduced in oocytes before the progression to MII and thus indicates that the transition into interphase is directly associated with the delayed triggering of anaphase I. Moreover, the defect(s) that initiate activation occur upstream of MAPK, as suppression of PKC activity failed to prevent activation by Mos(tm1Ev)/Mos(tm1Ev) LTXBO oocytes expressing no detectable MAPK activity. In summary, PKC participates in the regulatory mechanisms that delay entry into anaphase I in LTXBO oocytes, and the disruption promotes untimely entry into interphase. Thus, loss of regulatory control over PKC activity during oocyte maturationdisrupts the critical MI-to-Mn transition, leading to a precocious exit from meiosis. (C) 2001 Academic Press.

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Documento generato il 30/10/20 alle ore 09:56:22