During early embryonic development, IP3- Ca2+ signaling transduces ventral signaling at the time of dorsoventral axis formation. To identify molecules functioning upstream in this signal pathway, we examined effects of a panel of inhibitory antibodies against Gαq/11, Gαs/olf, or Gαi/o/t/z. While all these antibodies showed direct inhibition of their targets, their effects on redirection of the ventral mesoderm to a dorsal fate varied. Anti-Gαs/olf antibody showed strong induction of dorsal fate, anti-Gαi/o/t/z antibody did so weakly, and anti-Gαq/11 antibody was without effect. Injection of βARK, a Gβγ inhibitor, mimicked the dorsalizing effect of anti-Gαs/olf antibody, whereas injection of adenylyl cyclase inhibitors at a concentration which inhibited Gαs-coupled cAMP increase did not do so. The activation of Gαs-coupled receptor gave rise to Ca2+ transients. All these results suggest that activation of the Gαs-coupled receptor relays dorsoventral signal to Gβγ, which then stimulates PLCβ and then the IP3-Ca2+ system. This signaling pathway may play a crucial role in transducing ventral signals. (C) 2000 Academic Press.
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