| First Author | Plummer NW | Year | 2012 |
| Journal | Proc Natl Acad Sci U S A | Volume | 109 |
| Issue | 52 | Pages | 21366-71 |
| PubMed ID | 23236180 | Mgi Jnum | J:193170 |
| Mgi Id | MGI:5467861 | Doi | 10.1073/pnas.1219810110 |
| Citation | Plummer NW, et al. (2012) Development of the mammalian axial skeleton requires signaling through the Galpha(i) subfamily of heterotrimeric G proteins. Proc Natl Acad Sci U S A 109(52):21366-71 |
| abstractText | 129/SvEv mice with a loss-of-function mutation in the heterotrimeric G protein alpha-subunit gene Gnai3 have fusions of ribs and lumbar vertebrae, indicating a requirement for Galpha(i) (the "inhibitory" class of alpha-subunits) in somite derivatives. Mice with mutations of Gnai1 or Gnai2 have neither defect, but loss of both Gnai3 and one of the other two genes increases the number and severity of rib fusions without affecting the lumbar fusions. No myotome defects are observed in Gnai3/Gnai1 double-mutant embryos, and crosses with a conditional allele of Gnai2 indicate that Galpha(i) is specifically required in cartilage precursors. Penetrance and expressivity of the rib fusion phenotype is altered in mice with a mixed C57BL/6 x 129/SvEv genetic background. These phenotypes reveal a previously unknown role for G protein-coupled signaling pathways in development of the axial skeleton. |
