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Activator of G Protein Signaling 3 Null Mice: I. Unexpected Alterations in Metabolic and Cardiovascular Function

Department of Pharmacology and Experimental Therapeutics (J.B.B., K.L., E.L., K.J.V., S.M.L.), Louisiana State University Health Sciences Center, New Orleans, Louisiana 70112; Department of Internal Medicine (T.L.S.), Transgenic Animal Model Core, University of Michigan, Ann Arbor, Michigan 48109; Division of Experimental Obesity (C.B., T.W.G.), Pennington Biomedical Research Center, Baton Rouge, Louisiana 70808; Department of Neurosciences (A.P.) and Department of Cell and Molecular Pharmacology and Experimental Therapeutics (J.B.B., S.M.L.), Medical University of South Carolina, Charleston, South Carolina 29425

Address all correspondence and requests for reprints to: Stephen M. Lanier, Ph.D., Colcock Hall, Medical University of South Carolina, Charleston, South Carolina 29425. E-mail: lanier{at}musc.edu.

Activator of G protein signaling (AGS)-3 plays functional roles in cell division, synaptic plasticity, addictive behavior, and neuronal development. As part of a broad effort to define the extent of functional diversity of AGS3-regulated-events in vivo, we generated AGS3 null mice. Surprisingly, AGS3 null adult mice exhibited unexpected alterations in cardiovascular and metabolic functions without any obvious changes in motor skills, basic behavioral traits, and brain morphology. AGS3 null mice exhibited a lean phenotype, reduced fat mass, and increased nocturnal energy expenditure. AGS3 null mice also exhibited altered blood pressure control mechanisms. These studies expand the functional repertoire for AGS3 and other G protein regulatory proteins providing unexpected mechanisms by which G protein systems may be targeted to influence obesity and cardiovascular function.