Neural tube defects and impaired neural progenitor cell proliferation in Gβ1-deficient mice

Hiroaki Okae, Yoichiro Iwakura

研究成果: Article

35 引用 (Scopus)

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Heterotrimeric G proteins are well known for their roles in signal transduction downstream of G protein-coupled receptors (GPCRs), and both Gα subunits and tightly associated Gβγ subunits regulate downstream effector molecules. Compared to Gα subunits, the physiological roles of individual Gβ and Gγ subunits are poorly understood. In this study, we generated mice deficient in the Gβ1 gene and found that Gβ1 is required for neural tube closure, neural progenitor cell proliferation, and neonatal development. About 40% Gβ1-/- embryos developed neural tube defects (NTDs) and abnormal actin organization was observed in the basal side of neuroepithelium. In addition, Gβ1-/- embryos without NTDs showed microencephaly and died within 2 days after birth. GPCR agonist-induced ERK phosphorylation, cell proliferation, and cell spreading, which were all found to be regulated by Gαi and Gβγ signaling, were abnormal in Gβ1-/- neural progenitor cells. These data indicate that Gβ1 is required for normal embryonic neurogenesis.

元の言語English
ページ(範囲)1089-1101
ページ数13
ジャーナルDevelopmental Dynamics
239
発行部数4
DOI
出版物ステータスPublished - 2010 4 1
外部発表Yes

ASJC Scopus subject areas

  • Developmental Biology

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