The sequence reported in this article has been deposited in the GenBank database (accession number DQ115398).
Original Article
xRic-8 is a GEF for Gsα and participates in maintaining meiotic arrest in Xenopus laevis oocytes†
Article first published online: 24 OCT 2007
DOI: 10.1002/jcp.21257
Copyright © 2007 Wiley-Liss, Inc.
Additional Information
How to Cite
Romo, X., Pastén, P., Martínez, S., Soto, X., Lara, P., de Arellano, A. R., Torrejón, M., Montecino, M., Hinrichs, M. V. and Olate, J. (2008), xRic-8 is a GEF for Gsα and participates in maintaining meiotic arrest in Xenopus laevis oocytes. J. Cell. Physiol., 214: 673–680. doi: 10.1002/jcp.21257
- †
Publication History
- Issue published online: 20 DEC 2007
- Article first published online: 24 OCT 2007
- Manuscript Accepted: 20 JUL 2007
- Manuscript Received: 27 APR 2007
Funded by
- CONICYT. Grant Number: PBCT ACT-44
- Abstract
- Article
- References
- Cited By
Abstract
Immature stage VI Xenopus oocytes are arrested at the G2/M border of meiosis I until exposed to progesterone, which induces meiotic resumption through a non-genomic mechanism. One of the earliest events produced by this hormone is inhibition of the plasma membrane enzyme adenylyl cyclase (AC), with the concomitant drop in intracellular cAMP levels and reinitiation of the cell cycle. Recently Gsα and Gβγ have been shown to play an important role as positive regulators of Xenopus oocyte AC, maintaining the oocyte in the arrested state. However, a question that still remains unanswered, is how the activated state of Gsα and Gβγ is achieved in the immature oocyte, since no receptor or ligand have been found to be required. Here we provide evidence that xRic-8 can act in vitro and in vivo as a GEF for Gsα. Overexpression of xRic-8, through mRNA injection, greatly inhibits progesterone induced oocyte maturation and endogenous xRic-8 mRNA depletion, through siRNA microinjection, induces spontaneous oocyte maturation. These results suggest that xRic-8 is participating in the immature oocyte by keeping Gsα-Gβγ-AC signaling complex in an activated state and therefore maintaining G2 arrest. J. Cell. Physiol. 214: 673–680, 2008. © 2007 Wiley-Liss, Inc.

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