A role for the MEK-MAPK pathway in okadaic acid-induced meiotic resumption of incompetent growing mouse oocytes.

Fully grown competent mouse oocytes spontaneously resume meiosis in vitro when released from their follicular environment, in contrast to growing incompetent oocytes, which remain blocked in prophase I. The cell cycle regulators, maturation promoting factor (MPF; [p34(cdc2)/cyclin B kinase]) and mitogen-activated protein (MAP) kinases (p42(MAPK) and p44(MAPK)), are implicated in meiotic competence acquisition. Incompetent oocytes contain levels of p42(MAPK), p44(MAPK), and cyclin B proteins that are comparable to those in competent oocytes, but their level of p34(cdc2) is markedly lower.

Acquisition of meiotic competence in growing mouse oocytes is controlled at both translational and posttranslational levels.

Full-grown mouse oocytes spontaneously resume meiosis in vitro when released from their follicular environment. By contrast, growing oocytes are not competent to resume meiosis; the molecular basis of meiotic competence is not known. Entry into M phase of the eukaryotic cell cycle is controlled by MPF, a catalytically active complex comprising p34cdc2 kinase and cyclin B.

Ribosomal S6 kinase p90rsk and mRNA cap-binding protein eIF4E phosphorylations correlate with MAP kinase activation during meiotic reinitiation of mouse oocytes.

During meiotic reinitiation of the mouse oocyte, entry into M-phase is regulated by changes of protein phosphorylation and by the stimulation of selective mRNA translation following the nuclear membrane dissolution. Our results reveal that M-phase kinases (MAP kinase and histone H1 kinase) are being activated together with S6 kinase and with the phosphorylation of eIF4E, the cap-binding subunit of the initiation factor eIF-4F. In order to test which signaling pathway(s) is(are) involved, okadaic acid and cycloheximide have been used as tools for differentially modulating MAP and histone H1 kinase activities.

An accumulation of p34cdc2 at the end of mouse oocyte growth correlates with the acquisition of meiotic competence.

Growing incompetent mouse oocytes released from follicular cells are unable to spontaneously resume meiosis in vitro. To identify the reasons for meiotic incompetence in these cells, the levels of p34cdc2/cyclin B kinase and p42MAPK between incompetent and competent oocytes were compared. p34cdc2 was present at very low levels in incompetent oocytes and accumulated abruptly at the time of meiotic competence acquisition.

Human seminal plasma inhibits brain nitric oxide synthase activity.

Nitric oxide is a chemical messenger which functions as a neurotransmitter or as a cytotoxic agent. Nitric oxide synthase (NOS) has been isolated from various mammalian reproductive tissues. The presence or absence of NOS in spermatozoa has not yet been reported.