| First Author | Jeong SJ | Year | 2013 |
| Journal | PLoS One | Volume | 8 |
| Issue | 7 | Pages | e68781 |
| PubMed ID | 23874761 | Mgi Jnum | J:225192 |
| Mgi Id | MGI:5691675 | Doi | 10.1371/journal.pone.0068781 |
| Citation | Jeong SJ, et al. (2013) GPR56 functions together with alpha3beta1 integrin in regulating cerebral cortical development. PLoS One 8(7):e68781 |
| abstractText | Loss of function mutations in GPR56, which encodes a G protein-coupled receptor, cause a specific human brain malformation called bilateral frontoparietal polymicrogyria (BFPP). Studies from BFPP postmortem brain tissue and Gpr56 knockout mice have previously showed that GPR56 deletion leads to breaches in the pial basement membrane (BM) and neuronal ectopias during cerebral cortical development. Since alpha3beta1 integrin also plays a role in pial BM assembly and maintenance, we evaluated whether it functions together with GPR56 in regulating the same developmental process. We reveal that loss of alpha3 integrin enhances the cortical phenotype associated with Gpr56 deletion, and that neuronal overmigration through a breached pial BM occurs earlier in double knockout than in Gpr56 single knockout mice. These observations provide compelling evidence of the synergism of GPR56 and alpha3beta1 integrin in regulating the development of cerebral cortex. |
