Evidence that protein kinase C (PKC) participates in the meiosis I to meiosis II transition in mouse oocytes.

Document Type

Article

Publication Date

2001

Keywords

Cells-Cultured, Immunohistochemistry, Indoles, Interphase, Isoenzymes, MAP-Kinase-Signaling-System, Maleimides, Maturation-Promoting-Factor, Meiosis, Metaphase, Mice, Mice-Inbred-C57BL, Microscopy-Confocal, Oocytes, Phenotype, Prophase, Protein-Kinase-C, SUPPORT-U-S-GOVT-P-H-S, Time-Factors, Transcription-Genetic

First Page

330

Last Page

342

JAX Source

Dev Biol 2001 Jul; 235(2):330-42.

Grant

CA34196/CA/NCI, CA62392/CA/NCI

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 X 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 entry into 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 maturation disrupts the critical MI-to-MII transition, leading to a precocious exit from meiosis. Copyright 2001 Academic Press.

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