P85 regulates neuronal migration through affecting neuronal morphology during mouse corticogenesis
In mammalian developing embryonic cortex, projection neurons migrate from the ventricular zone to the cortical plate, guided by radial glial cells with a transformation between bipolar and multipolar morphology. Previous studies have demonstrated that the PI3K-Akt-mTOR signal plays a critical role in brain development. However, the function of P85 in cortical development is still unclear. In the present study, we found that overexpression of P85 impaired cortical neuronal migration. Using in utero electroporation, we revealed that the length of the leading process in P85 overexpressed neurons became shorter than that in the control group but with more branches. Using markers for new-born neurons, we further found that overexpression of P85 did not affect the ultimate fate of these cortical neurons. These findings indicated that the P85 subunit plays an essential role in neuronal migration and neuronal morphology during mouse corticogenesis.
KeywordsP85 In utero electroporation Neuronal migration Neurite growth Fate determination
This work was supported by the National Natural Science Foundation of China (NSFC) (No. 31572477) and Resource-based Industry Key Technology of Shaanxi Province (No.2016KTCL02-19). We appreciate Yanqing Wang for assistance with the laser scanning confocal microscope and Life Science Research Core Service (LSRCS) at Northwest A&F University.
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Conflict of interest
The authors declare that they have no conflict of interest.