GSBS Student Publications


xRic-8 is a GEF for Gsalpha and participates in maintaining meiotic arrest in Xenopus laevis oocytes

UMMS Affiliation

Departamento de Bioquimica y Biologia Molecular; Department of Cell Biology



Document Type


Medical Subject Headings

Amino Acid Sequence; Animals; Base Sequence; Cloning, Molecular; GTP-Binding Protein alpha Subunits, Gs; Gene Expression Regulation; Guanine Nucleotide Exchange Factors; Humans; *Meiosis; Molecular Sequence Data; Oocytes; RNA, Messenger; RNA, Small Interfering; Xenopus Proteins; Xenopus laevis


Life Sciences | Medicine and Health Sciences


Immature stage VI Xenopus oocytes are arrested at the G(2)/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 Gsalpha and Gbetagamma 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 Gsalpha and Gbetagamma 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 Gsalpha. 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 Gsalpha-Gbetagamma-AC signaling complex in an activated state and therefore maintaining G2 arrest.

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Citation: J Cell Physiol. 2008 Mar;214(3):673-80. Link to article on publisher's site

DOI of Published Version


Related Resources

Link to Article in PubMed

Journal Title

Journal of cellular physiology

PubMed ID