Gαq splice variants mediate phototransduction, rhodopsin synthesis, and retinal integrity in .

Heterotrimeric G proteins mediate a variety of signaling processes by coupling G protein-coupled receptors to intracellular effector molecules. In the α gene encodes several Gαq splice variants, with the Gαq1 isoform protein playing a major role in fly phototransduction. However, α null mutant flies still exhibit a residual light response, indicating that other Gαq splice variants or additional Gq α subunits are involved in phototransduction. Here, we isolated a mutant fly with no detectable light responses, decreased rhodopsin (Rh) levels, and rapid retinal degeneration. Using electrophysiological and genetic studies, biochemical assays, immunoblotting, real-time RT-PCR, and EM analysis, we found that mutations in the α gene disrupt light responses and demonstrate that the Gαq3 isoform protein is responsible for the residual light response in α null mutants. Moreover, we report that Gαq3 mediates rhodopsin synthesis. Depletion of all Gαq splice variants led to rapid light-dependent retinal degeneration, due to the formation stable Rh1-arrestin 2 (Arr2) complexes. Our findings clarify essential roles of several different Gαq splice variants in phototransduction and retinal integrity in and reveal that Gαq3 functions in rhodopsin synthesis.