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. 2017 Nov 1;144(21):4002–4014. doi: 10.1242/dev.147934

Fig. 5.

Fig. 5.

Paxillin deficiency in post-mitotic neurons disrupts neuronal positioning. (A) Representative sections of littermate control (PxnF/F) and mutant (NEX-Cre:PxnF/F), with a conditional deletion of paxillin in post-mitotic immature neurons, were immunostained for Cux1 (green). More Cux1+ neurons were found in ectopic deep positions in the mutant cortex (arrow). (B) Box-and-whisker plot distribution of positions of Cux1+ neurons. The mutant showed a broader distribution compared with littermate controls. The mean position of Cux1+ neurons was significantly deeper in the mutant cortex (n=3 in PxnF/F and n=4 in NEX-Cre:PxnF/F). (C) Representative images of Tle4+ (red) and Ctip2+ (green) neurons. (D) Distribution of Tbr1+ (n=3 in PxnF/F and n=4 in NEX-Cre:PxnF/F), Tle4+ (n=3 in PxnF/F and n=4 in NEX-Cre:PxnF/F) and Ctip2+ (n=3 in PxnF/F and n=4 in NEX-Cre:PxnF/F) neurons. There was no difference in the mean positions of the Tbr1+, Tle4+ and Ctip2+ neurons between the genotypes. ***P<0.001. Scale bars: 50 µm.