Meiotic resumption in response to luteinizing hormone is independent of a Gi family G protein or calcium in the mouse oocyte |
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Authors: | Mehlmann Lisa M Kalinowski Rebecca R Ross Lavinia F Parlow Albert F Hewlett Erik L Jaffe Laurinda A |
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Affiliation: | Department of Cell Biology, University of Connecticut Health Center, 263 Farmington Ave., Farmington, CT 06032, USA. lmehlman@neuron.uchc.edu |
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Abstract: | The signaling pathway by which luteinizing hormone (LH) acts on the somatic cells of vertebrate ovarian follicles to stimulate meiotic resumption in the oocyte requires a decrease in cAMP in the oocyte, but how cAMP is decreased is unknown. Activation of Gi family G proteins can lower cAMP by inhibiting adenylate cyclase or stimulating a cyclic nucleotide phosphodiesterase, but we show here that inhibition of this class of G proteins by injection of pertussis toxin into follicle-enclosed mouse oocytes does not prevent meiotic resumption in response to LH. Likewise, elevation of Ca2+ can lower cAMP through its action on Ca2+-sensitive adenylate cyclases or phosphodiesterases, but inhibition of a Ca2+ rise by injection of EGTA into follicle-enclosed mouse oocytes does not inhibit the LH response. Thus, neither of these well-known mechanisms of cAMP regulation can account for LH signaling to the oocyte in the mouse ovary. |
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Keywords: | Meiotic resumption Oocyte maturation Luteinizing hormone Heterotrimeric G proteins Intracellular calcium Follicle-enclosed oocytes Mouse |
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