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Fig. 5 | Molecular Autism

Fig. 5

From: Autism-associated CHD8 deficiency impairs axon development and migration of cortical neurons

Fig. 5

CHD8 regulates the axon growth in vivo. ai Representative images of coronal slices of P3 mouse brains that were transfected with GFP together with indicated constructs by in utero electroporation at E14.5. High-magnification images are shown in the right. Brain slices at the level of Bregma − 1.58 mm were stained with Hoechst and GFP antibodies to visualize the callosal. Scale bar, 150 μm (a, d, g), 200 μm (b, e, h), or 400 μm (c, f, i). j A schematic for quantitative analysis of callosal axon length. The adjacent axon lengths were measured from the midline to end. k Quantitative analysis of callosal axon length Chd8 ShRNA#2 construct showed significantly shorter axonal length than scramble control. The co-expression of human hCHD8 rescued the phenotypes caused by knockdown of Chd8 by shRNA#2 construct. Distance from the midline: shRNA-scr, 3763 ± 154.3 μm; shRNA#2, 1563 ± 47.95 μm. ***P < 0.0001 shRNA#2 vs shRNA-scr; shRNA#-hCHD8, 2575 ± 307.2 μm. **P = 0.0021 shRNA#2-hCHD8 vs shRNA-scr. Results are shown as mean ± SEM. n = 4 in each group. For ANOVA, P = 0.0016. For Bonferroni post-tests, **P < 0.01; ***P < 0.001

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