Embryonic cardiomyocyte hypoplasia and craniofacial defects in Gα(q)/Gα11-mutant mice

Stefan Offermanns, Li Ping Zhao, Antje Gohla, Ildiko Sarosi, Melvin I. Simon, Thomas M. Wilkie

Research output: Contribution to journalArticlepeer-review

191 Scopus citations

Abstract

Heterotrimeric G proteins of the G(q) class have been implicated in signaling pathways regulating cardiac growth under physiological and pathological conditions. Knockout mice carrying inactivating mutations in both of the widely expressed Gα(q) class genes, Gα(q) and Gα11, demonstrate that at least two active alleles of these genes are required for extrauterine life. Mice carrying only one intact allele [Gα(q)((-/+));Gα11((-/-)) or Gα(q)((-/-));Gα11((-/+))] died shortly after birth. These mutants showed a high incidence of cardiac malformation. In addition, Gα(q)((-/-));Gα11((-/+)) newborns suffered from craniofacial defects. Mice lacking both Gα(q) and Gα11 [Gα(q)((-/-));Gα11((-/-))] died at embryonic day 11 due to cardiomyocyte hypoplasia. These data demonstrate overlap in Gα(q) and Gα11 gene functions and indicate that the G(q) class of G proteins plays a crucial role in cardiac growth and development.

Original languageEnglish (US)
Pages (from-to)4304-4312
Number of pages9
JournalEMBO Journal
Volume17
Issue number15
DOIs
StatePublished - Aug 3 1998

Keywords

  • Cardiac malformation
  • Craniofacial defect
  • G protein
  • Heart defect
  • Knockout

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

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