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

doi:10.1093/emboj/17.15.4304

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 journal › Article › peer-review

204 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 language	English (US)
Pages (from-to)	4304-4312
Number of pages	9
Journal	EMBO Journal
Volume	17
Issue number	15
DOIs	https://doi.org/10.1093/emboj/17.15.4304
State	Published - 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)

Access to Document

10.1093/emboj/17.15.4304

Cite this

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

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.",

keywords = "Cardiac malformation, Craniofacial defect, G protein, Heart defect, Knockout",

author = "Stefan Offermanns and Zhao, {Li Ping} and Antje Gohla and Ildiko Sarosi and Simon, {Melvin I.} and Wilkie, {Thomas M.}",

year = "1998",

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T1 - Embryonic cardiomyocyte hypoplasia and craniofacial defects in Gα(q)/Gα11-mutant mice

AU - Offermanns, Stefan

AU - Zhao, Li Ping

AU - Gohla, Antje

AU - Sarosi, Ildiko

AU - Simon, Melvin I.

AU - Wilkie, Thomas M.

PY - 1998/8/3

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N2 - 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.

AB - 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.

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