| First Author | Guo Y | Year | 2017 |
| Journal | Cereb Cortex | Volume | 27 |
| Issue | 6 | Pages | 3414-3426 |
| PubMed ID | 28334111 | Mgi Jnum | J:242591 |
| Mgi Id | MGI:5905701 | Doi | 10.1093/cercor/bhx042 |
| Citation | Guo Y, et al. (2017) Gbeta2 Regulates the Multipolar-Bipolar Transition of Newborn Neurons in the Developing Neocortex. Cereb Cortex 27(6):3414-3426 |
| abstractText | Proper neuronal migration is critical for the formation of the six-layered neocortex in the mammalian brain. However, the precise control of neuronal migration is not well understood. Heterotrimeric guanine nucleotide binding proteins (G proteins), composed of Galpha and Gbetagamma, transduce signals from G protein-coupled receptors to downstream effectors and play crucial roles in brain development. However, the functions of individual subunits of G proteins in prenatal brain development remain unclear. Here, we report that Gbeta2 is expressed in the embryonic neocortex, with abundant expression in the intermediate zone, and is significantly upregulated in differentiated neurons. Perturbation of Gbeta2 expression impairs the morphogenetic transformation of migrating neurons from multipolar to bipolar and subsequently delays neuronal migration. Moreover, Gbeta2 acts as a scaffold protein to organize the MP1-MEK1-ERK1/2 complex and mediates the phosphorylation of ERK1/2. Importantly, expression of a constitutively active variant of MEK1 rescues the migration defects that are caused by the loss of Gbeta2. In conclusion, our findings reveal that Gbeta2 regulates proper neuronal migration during neocortex development by activating the ERK1/2 signaling pathway. |
