Gαs family G proteins activate IP3-Ca2+ signaling via Gβγ and transduce ventralizing signals in Xenopus

Shoen Kume, Takafumi Inoue, Katsuhiko Mikoshiba

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)88-103
Number of pages16
JournalDevelopmental Biology
Volume226
Issue number1
DOIs
Publication statusPublished - 2000 Oct 1
Externally publishedYes

Fingerprint

Xenopus
GTP-Binding Proteins
Antibodies
Injections
Mesoderm
Embryonic Development
Signal Transduction

Keywords

  • Ca
  • Dorsoventral axis
  • G proteins
  • IP
  • Xenopus

ASJC Scopus subject areas

  • Developmental Biology

Cite this

Gαs family G proteins activate IP3-Ca2+ signaling via Gβγ and transduce ventralizing signals in Xenopus. / Kume, Shoen; Inoue, Takafumi; Mikoshiba, Katsuhiko.

In: Developmental Biology, Vol. 226, No. 1, 01.10.2000, p. 88-103.

Research output: Contribution to journalArticle

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