| First Author | Zhang JH | Year | 2011 |
| Journal | J Neurochem | Volume | 119 |
| Issue | 3 | Pages | 544-54 |
| PubMed ID | 21883221 | Mgi Jnum | J:177473 |
| Mgi Id | MGI:5295142 | Doi | 10.1111/j.1471-4159.2011.07457.x |
| Citation | Zhang JH, et al. (2011) Knockout of G protein beta5 impairs brain development and causes multiple neurologic abnormalities in mice. J Neurochem 119(3):544-54 |
| abstractText | Gbeta5 is a divergent member of the signal-transducing G protein beta subunit family encoded by GNB5 and expressed principally in brain and neuronal tissue. Among heterotrimeric Gbeta isoforms, Gbeta5 is unique in its ability to heterodimerize with members of the R7 subfamily of the regulator of G protein signaling proteins that contain G protein-gamma like domains. Previous studies employing Gnb5 knockout (KO) mice have shown that Gbeta5 is an essential stabilizer of such regulator of G protein signaling proteins and regulates the deactivation of retinal phototransduction and the proper functioning of retinal bipolar cells. However, little is known of the function of Gbeta5 in the brain outside the visual system. We show here that mice lacking Gbeta5 have a markedly abnormal neurologic phenotype that includes impaired development, tiptoe-walking, motor learning and coordination deficiencies, and hyperactivity. We further show that Gbeta5-deficient mice have abnormalities of neuronal development in cerebellum and hippocampus. We find that the expression of both mRNA and protein from multiple neuronal genes is dysregulated in Gnb5 KO mice. Taken together with previous observations from Gnb5 KO mice, our findings suggest a model in which Gbeta5 regulates dendritic arborization and/or synapse formation during development, in part by effects on gene expression. |
