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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 α3β1 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 α3 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 α3β1 integrin in regulating the development of cerebral cortex.

GPR56 Functions Together with α3β1 Integrin in Regulating Cerebral Cortical Development