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Molecular and Cellular Biology, September 2004, p. 7758-7768, Vol. 24, No. 17
0270-7306/04/$08.00+0     DOI: 10.1128/MCB.24.17.7758-7768.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

Mice with Deficiency of G Protein ₃ Are Lean and Have Seizures

Weis Center for Research, Geisinger Clinic, Danville,¹ Department of Cellular and Molecular Physiology, The Pennsylvania State College of Medicine, Hershey, Pennsylvania,³ Department of Pharmacology and Toxicology, Virginia Commonwealth University, Richmond, Virginia²

Received 26 February 2004/ Returned for modification 3 April 2004/ Accepted 13 June 2004

Emerging evidence suggests that the subunit composition of an individual G protein contributes to the specificity of the hundreds of known receptor signaling pathways. Among the twelve subtypes, ₃ is abundantly and widely expressed in the brain. To identify specific functions and associations for ₃, a gene-targeting approach was used to produce mice lacking the Gng3 gene (Gng3^–/–). Confirming the efficacy and specificity of gene targeting, Gng3^–/– mice show no detectable expression of the Gng3 gene, but expression of the divergently transcribed Bscl2 gene is not affected. Suggesting unique roles for ₃ in the brain, Gng3^–/– mice display increased susceptibility to seizures, reduced body weights, and decreased adiposity compared to their wild-type littermates. Predicting possible associations for ₃, these phenotypic changes are associated with significant reductions in ß₂ and _i3 subunit levels in certain regions of the brain. The finding that the Gng3^–/– mice and the previously reported Gng7^–/– mice display distinct phenotypes and different ß subunit associations supports the notion that even closely related subtypes, such as ₃ and ₇, perform unique functions in the context of the organism.

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