title: Induction of maturation-promoting factor during Xenopus oocyte maturation uncouples Ca(2+) store depletion from store-operated Ca(2+) entry.
abstract: During oocyte maturation, eggs acquire the ability to generate specialized Ca(2+) signals in response to sperm entry. Such Ca(2+) signals are crucial for egg activation and the initiation of embryonic development. We examined the regulation during Xenopus oocyte maturation of store-operated Ca(2+) entry (SOCE), an important Ca(2+) influx pathway in oocytes and other nonexcitable cells. We have previously shown that SOCE inactivates during Xenopus oocyte meiosis. SOCE inactivation may be important in preventing premature egg activation. In this study, we investigated the correlation between SOCE inactivation and the Mos-mitogen-activated protein kinase (MAPK)-maturation-promoting factor (MPF) kinase cascade, which drives Xenopus oocyte maturation. SOCE inactivation at germinal vesicle breakdown coincides with an increase in the levels of MAPK and MPF. By differentially inducing Mos, MAPK, and MPF, we demonstrate that the activation of MPF is necessary for SOCE inactivation during oocyte maturation. In contrast, sustained high levels of Mos kinase and the MAPK cascade have no effect on SOCE activation. We further show that preactivated SOCE is not inactivated by MPF, suggesting that MPF does not block Ca(2+) influx through SOCE channels, but rather inhibits coupling between store depletion and SOCE activation.
authors.affiliation: Department of Physiology and Biophysics, University of Arkansas Medical Science, Little Rock, 72205, USA. machacakhaleda@uams.edu
authors.forename: Khaled
authors.initials: K
authors.lastname: Machaca
authors.forename: Shirley
authors.initials: S
authors.lastname: Haun
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000187:drug effects; D018797:Cell Cycle Proteins; D019926:Cyclin B / Q000235:genetics / Q000494:pharmacology; D056744:Cyclin B1; D022162:Cytoplasmic Vesicles / Q000378:metabolism*; D004594:Electrophysiology; D005260:Female; D020935:MAP Kinase Signaling System / Q000187:drug effects; D016200:Maturation-Promoting Factor / Q000378:metabolism*; D008564:Membrane Potentials / Q000187:drug effects; D020929:Mitogen-Activated Protein Kinase Kinases / Q000378:metabolism; D009154:Mutation; D009687:Nuclear Proteins; D009865:Oocytes / Q000166:cytology / Q000187:drug effects / Q000254:growth & development* / Q000378:metabolism*; D009866:Oogenesis; D011374:Progesterone / Q000494:pharmacology; D011505:Protein-Tyrosine Kinases / Q000378:metabolism / Q000494:pharmacology; D017231:Proto-Oncogene Proteins c-mos / Q000235:genetics / Q000378:metabolism / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D013997:Time Factors; D029867:Xenopus Proteins; D014982:Xenopus laevis / Q000502:physiology*
chemical_list: D018797:Cell Cycle Proteins; D019926:Cyclin B; D056744:Cyclin B1; D009687:Nuclear Proteins; D012333:RNA, Messenger; D029867:Xenopus Proteins; D011374:Progesterone; C530005:WEE1 protein, Xenopus; D011505:Protein-Tyrosine Kinases; D017231:Proto-Oncogene Proteins c-mos; D016200:Maturation-Promoting Factor; D020929:Mitogen-Activated Protein Kinase Kinases; D002118:Calcium