| First Author | Moon AM | Year | 2014 |
| Journal | PLoS One | Volume | 9 |
| Issue | 3 | Pages | e90970 |
| PubMed ID | 24599258 | Mgi Jnum | J:215128 |
| Mgi Id | MGI:5604689 | Doi | 10.1371/journal.pone.0090970 |
| Citation | Moon AM, et al. (2014) Disruption of G-protein gamma5 subtype causes embryonic lethality in mice. PLoS One 9(3):e90970 |
| abstractText | Heterotrimeric G-proteins modulate many processes essential for embryonic development including cellular proliferation, migration, differentiation, and survival. Although most research has focused on identifying the roles of the various alphasubtypes, there is growing recognition that similarly divergent betagamma dimers also regulate these processes. In this paper, we show that targeted disruption of the mouse Gng5 gene encoding the gamma5 subtype produces embryonic lethality associated with severe head and heart defects. Collectively, these results add to a growing body of data that identify critical roles for the gamma subunits in directing the assembly of functionally distinct G-alphabetagamma trimers that are responsible for regulating diverse biological processes. Specifically, the finding that loss of the G-gamma5 subtype is associated with a reduced number of cardiac precursor cells not only provides a causal basis for the mouse phenotype but also raises the possibility that G-betagamma5 dependent signaling contributes to the pathogenesis of human congenital heart problems. |
