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Journal of Neuroscience, Vol 16, 1317-1323, Copyright © 1996 by Society for Neuroscience
Gi-mediated stimulation of type II adenylyl cyclase is augmented by Gq- coupled receptor activation and phorbol ester treatment
RC Tsu and YH Wong
Department of Biology, Hong Kong University of Science and Technology, Clear Water Bay, Kowloon.
Synergism between Gs- and Gi- or Gq-dependent signaling pathways has been
demonstrated in the stimulation of type II adenylyl cyclase (AC- II).
Provision of activated alpha s is known to allow numerous Gi- coupled
receptors to stimulate AC-II and to potentiate the responses to Gq-coupled
receptors. To explore possible interactions between Gi- and Gq-coupled
receptors that are independent of alpha s, the activity of AC-II was
determined after the activation of Gi- and Gq-regulated pathways. Human
embryonic kidney 293 cells were transiently cotransfected with cDNAs
encoding AC-II and various G-protein-coupled receptors. Agonist-bound
Gi-coupled receptors (including the formyl peptide, dopamine-D2, and
delta-opioid receptors) stimulated AC-II activity in the absence of
activated alpha s, provided that the cells were treated with 100 nM phorbol
12-myristate 13-acetate. Activation of protein kinase C (PKC) thus appears
to relieve the requirement for the presence of activated alpha s.
Stimulation of PKC via Gq-coupled receptors also allowed Gi-coupled
receptors to activate AC-II. Coexpression of the m1 muscarinic receptor
with the dopamine-D2 receptor permitted dopamine to stimulate AC-II in the
presence of carbachol. The phorbol ester-permissive and alpha s-independent
stimulation was mediated by G-protein beta gamma subunits because it was
blocked by the beta gamma scavengers alpha t and beta-adrenergic receptor
kinase. These results show that AC-II can efficiently integrate signals
generated by Gq- and Gi-coupled receptors via a mechanism that is
independent of Gs.
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