1. xRic-8 is a GEF for Gsα and participates in maintaining meiotic arrest inXenopus laevis oocytes
- Author
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Antonieta Ramirez de Arellano, Ximena Romo, Silvana Martinez, Marcela Torrejón, Pamela Pasten, Pablo Lara, Ximena Soto, Juan Olate, María Victoria Hinrichs, and Martin Montecino
- Subjects
Gs alpha subunit ,Physiology ,Molecular Sequence Data ,Clinical Biochemistry ,Xenopus ,Xenopus Proteins ,Biology ,Adenylyl cyclase ,Xenopus laevis ,chemistry.chemical_compound ,GTP-Binding Protein alpha Subunits, Gs ,medicine ,Animals ,Guanine Nucleotide Exchange Factors ,Humans ,Amino Acid Sequence ,RNA, Messenger ,Cloning, Molecular ,RNA, Small Interfering ,Receptor ,Microinjection ,Base Sequence ,Cell Biology ,Cell cycle ,biology.organism_classification ,Oocyte ,Cell biology ,Meiosis ,medicine.anatomical_structure ,Gene Expression Regulation ,chemistry ,Oocytes ,Intracellular - 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.
- Published
- 2007