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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 

Meiotic resumption in response to luteinizing hormone is independent of a G(i) family G protein or calcium in the mouse oocyte.

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 G(i) 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 Ca(2+) can lower cAMP through its action on Ca(2+)-sensitive adenylate cyclases or phosphodiesterases, but inhibition of a Ca(2+) 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.[1]

References

  1. Meiotic resumption in response to luteinizing hormone is independent of a G(i) family G protein or calcium in the mouse oocyte. Mehlmann, L.M., Kalinowski, R.R., Ross, L.F., Parlow, A.F., Hewlett, E.L., Jaffe, L.A. Dev. Biol. (2006) [Pubmed]
 
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