Stimulation of Xenopus oocyte maturation by inhibition of the G-protein alpha S subunit, a component of the plasma membrane and yolk platelet membranes.

Abstract

Abstract. Oocytes of Xenopus laevis undergo maturation when injected with an affinity-purified antibody against the COOH-terminal decapeptide of the et subunit of the G-protein Gs, an antibody that inhibits Gs activity. Germinal vesicle breakdown, chromosome condensation, and polar body formation occur, with a time course similar to that for oocytes treated with progesterone. The as antibody-injected oocytes also acquire the ability to be activated by sperm. Coinjection of the catalytic subunit of cAMP-dependent protein kinase, or incubation with cycloheximide, inhibits maturation in response to injection of the eq antibody; these experiments show that the as antibody acts at an early point in the pathway leading to oocyte maturation, before formation of maturation promoting factor, and like progesterone, its action requires protein synthesis. Immunogold electron microscopy shows that as is present in the yolk platelet membranes as well as the plasma membrane. These results support the hypothesis that progesterone acts by inhibiting oq, and suggest that the target of progesterone could include yolk platelet membranes as well as the plasma membrane.

Expression of G protein estrogen receptor (GPER) on membrane of mouse oocytes during maturation

“…A major intracellular signaling cascade family implicated in the mitogen-activated protein kinase (MAPK) pathways [20,21] plays important roles during the meiotic maturation of oocytes. Inhibition of the G-protein alpha S subunit stimulates xenopus oocyte maturation, suggesting that G-proteins also involved in oocyte maturation [22]. From the results of the presence of GPER on the oocyte membrane indicate that GPER may relate to the oocyte maturation process.…”

Gβγ signaling reduces intracellular cAMP to promote meiotic progression in mouse oocytes

“…Evidence supporting this model is plentiful, including the following: First, steroids trigger a rapid decrease in intracellular cAMP with a concomitant decrease in PKA activity [9][10][11][12]. Second, over-expression of either Gα s or Gβγ inhibits steroid-triggered oocyte maturation, while reduction of Gα s or Gβγ levels or activity leads to enhanced maturation in response to steroids [13][14][15][16]. Third, stimulation of overexpressed Gα s -or Gβγ-coupled receptors markedly inhibits steroid-triggered oocyte maturation [17,18].…”

Molecular characterization of three forms of putative membrane-bound progestin receptors and their tissue-distribution in channel catfish, Ictalurus punctatus

“…The precise mechanism for the activation and/or stabilization of the maturationpromoting factor by the maturation-inducing steroid (MIS) appears to differ among species. For example, the MIS-receptor (MIS-R), which in fish is a membranebound progestin receptor (mPR), appears to be coupled to an inhibitory G-protein (Gi) in three fish species: rainbow trout, Atlantic croaker and spotted seatrout, (Yoshikuni & Nagahama 1994, Thomas et al 2002, Zhu et al 2003a, whereas in zebrafish and an amphibian, Xenopus, it is likely that progestins activate a stimulatory G-protein (Gallo et al 1995, Kalinowski et al 2004. However, many other processes initiated through activation of the membrane-bound MIS-R, such as a decrease in intracellular cAMP levels, have been shown to be conserved (Yamashita et al 2000).…”