AN EYE-SPECIFIC G-BETA SUBUNIT ESSENTIAL FOR TERMINATION OF THE PHOTOTRANSDUCTION CASCADE

HETEROTRIMERIC G proteins couple various receptors to intracellular ef fector molecules. Although the role of the G alpha subunit in effector activation, guanine nucleotide exchange and GTP hydrolysis has been w ell studied(1-4), the cellular functions of the G beta subunits are le ss well understood(5,6). G beta gamma dimers bind G alpha subunits and anchor them to the membrane for presentation to the receptor(7,9). Tn specific systems, the G beta subunits have also been implicated in di rect coupling to ion channels and to effector molecules(10-19). We hav e isolated Drosophila melanogaster mutants defective in an eye-specifi c G-protein beta-subunit (G beta e), and show here that the beta-subun it is essential for G-protein-receptor coupling in vivo. Remarkably, G beta mutants are also severely defective in the deactivation of the l ight response, demonstrating an essential role for the G beta subunit in terminating the active state of this signalling cascade.