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Volume 582, Issue 27, Pages 3783-3787 (12 November 2008)


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Tonic activity of Gα-gustducin regulates taste cell responsivity

Edited by Jesus Avila

Tod R. Clappab, Kristina R. Trubeyc, Aurelie Vandenbeuchab, Leslie M. Stoneab, Robert F. Margolskeee, Nirupa Chaudharicd1, Sue C. KinnamonabCorresponding Author Information1email address

Received 28 August 2008; received in revised form 3 October 2008; accepted 6 October 2008. published online 17 October 2008.

Abstract 

The taste-selective G protein, α-gustducin (α-gus) is homologous to α-transducin and activates phosphodiesterase (PDE) in vitro. α-Gus-knockout mice are compromized to bitter, sweet and umami taste stimuli, suggesting a central role in taste transduction. Here, we suggest a different role for Gα-gus. In taste buds of α-gus-knockout mice, basal (unstimulated) cAMP levels are high compared to those of wild-type mice. Further, H-89, a cAMP-dependent protein kinase inhibitor, dramatically unmasks responses to the bitter tastant denatonium in gus-lineage cells of knockout mice. We propose that an important role of α-gus is to maintain cAMP levels tonically low to ensure adequate Ca2+ signaling.

a Department of Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, United States

b Rocky Mountain Taste and Smell Center, University of Colorado Denver, Aurora, CO 80045, United States

c Department of Physiology and Biophysics, University of Miami Miller School of Medicine, Miami, FL 33136, United States

d Program in Neurosciences, University of Miami Miller School of Medicine, Miami, FL 33136, United States

e Department of Neuroscience, Mount Sinai School of Medicine, New York, NY 10029, United States

Corresponding Author InformationCorresponding author. Address: Department of Biomedical Sciences, Colorado State University, Fort Collins, CO 80523, United States. Fax: +1 970 491 7907.

1 These authors contributed equally to the work.

PII: S0014-5793(08)00823-5

doi:10.1016/j.febslet.2008.10.007


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