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A Gβγ stimulated adenylyl cyclase is involved in xenopus laevis oocyte maturation
Author(s) -
Guzmán Leonardo,
Romo Ximena,
Grandy Rodrigo,
Soto Ximena,
Montecino Martín,
Hinrichs Maríavictoria,
Olate Juan
Publication year - 2005
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.20102
Subject(s) - xenopus , oocyte , microinjection , adenylyl cyclase , biology , minigene , microbiology and biotechnology , gene isoform , gs alpha subunit , signal transduction , gene , genetics , alternative splicing , embryo
Xenopus laevis oocyte maturation is induced by the steroid hormone progesterone through a nongenomic mechanism that implicates the inhibition of the effector system adenylyl cyclase (AC). Recently, it has been shown that the G protein βγ heterodimer is involved in oocyte maturation arrest. Since AC is the proposed target for Gβγ action, we considered of importance to identify and characterize the Gβγ regulated AC isoform(s) that are expressed in the Xenopus oocyte. Through biochemical studies, we found that stage VI plasma membrane oocyte AC activity showed attributes of an AC2 isoform. Furthermore, exogenous Gβγ was capable to activate oocyte AC only in the presence of the activated form of Gαs (Gαs‐GTPγS), which is in agreement with the Gγβ conditional activation reported for the mammalian AC2 and AC4 isotypes. In order to study the functional role of AC in oocyte maturation we cloned from a Xenopus oocyte cDNA library a gene encoding an AC with high identity to AC7 (xAC7). Based on this sequence, we constructed a minigene encoding the AC‐Gβγ interacting region (xAC7pep) to block, within the oocyte, this interaction. We found that microinjection of the xAC7pep potentiated progesterone‐induced maturation, as did the AC2 minigene. From these results we can conclude that a Gβγ‐activated AC is playing an important role in Xenopus oocyte meiotic arrest in a Gαs‐GTP dependent manner. © 2005 Wiley‐Liss, Inc.