学術雑誌論文

学術雑誌論文

text

PLOS ONE. 2013, 8(7), p. e68781

GPR56 Functions Together with α3β1 Integrin in Regulating Cerebral Cortical Development

PLOS

英語

text

2013-07

https://doi.org/10.1371/journal.pone.0068781

Jeong S-J, Luo R, Singer K, Giera S, Kreidberg J, Kiyozumi D, et al. (2013) GPR56 Functions Together with α3β1 Integrin in Regulating Cerebral Cortical Development. PLoS ONE 8(7): e68781. https://doi.org/10.1371/journal.pone.0068781

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.

© 2013 Jeong et al. This article is licensed under a Creative Commons Attribution 4.0 International License.

71798

GPR56 Functions Together with α3β1 Integrin in Regulating Cerebral Cortical Development

PLOS

英語

2013-07

PLOS ONE

8

7

e68781

https://doi.org/10.1371/journal.pone.0068781

https://hdl.handle.net/11094/71798