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Molecular and Cellular Biology, May 2005, p. 4221-4228, Vol. 25, No. 10
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.10.4221-4228.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Generation and Characterization of Rgs4 Mutant Mice

Nicolas Grillet,1 Alexandre Pattyn,1 Candice Contet,2 Brigitte L. Kieffer,2 Christo Goridis,1 and Jean-François Brunet1*

CNRS UMR 8542, Department of Biology, Ecole Normale Supérieure, Paris, France,1 Institut de Génétique et de Biologie Moleculaire et Cellulaire, Illkirch, France2

Received 10 November 2004/ Returned for modification 21 January 2005/ Accepted 26 February 2005

RGS proteins are negative regulators of signaling through heterotrimeric G protein-coupled receptors and, as such, are in a position to regulate a plethora of biological phenomena. However, those have just begun to be explored in vivo. Here, we describe a mouse line deficient for Rgs4, a gene normally expressed early on in discrete populations of differentiating neurons and later on at multiple sites of the central nervous system, the cortex in particular, where it is one of the most highly transcribed Rgs genes. Rgs4lacZ/lacZ mice had normal neural development and were viable and fertile. Behavioral testing on mutant adults revealed subtle sensorimotor deficits but, so far, supported neither the proposed status of Rgs4 as a schizophrenia susceptibility gene (by showing intact prepulse inhibition in the mutants) nor (unlike another member of the Rgs family, Rgs9) a role of Rgs4 in the acute or chronic response to opioids.

* Corresponding author. Mailing address: CNRS UMR 8542, Ecole normale supérieure, 46 rue d'Ulm, 75005, Paris, France. Phone: 33 1 44 32 23 21. Fax: 33 1 44 32 23 23. E-mail: jfbrunet{at}biologie.ens.fr.

Molecular and Cellular Biology, May 2005, p. 4221-4228, Vol. 25, No. 10
0022-538X/05/$08.00+0     doi:10.1128/MCB.25.10.4221-4228.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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