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. Author manuscript; available in PMC: 2017 Nov 23.
Published in final edited form as: Neuron. 2016 Oct 27;92(4):813–828. doi: 10.1016/j.neuron.2016.09.056

Figure 7. Loss of Wdr62 and Aspm disrupts apical complex proteins and leads to premature dissociation of ciliary remnants from centrosomes.

Figure 7

(A) Reduction in centrosomes and cilia in the Wdr62 −/− mouse brain, both at and away from the ventricular surface, along with an increase in dissociated ciliary remnants. Shown here are E12.5 WT (top) and Wdr62 −/− (bottom) brain sections immunostained for γ-tubulin (centrosomes) and Arl13b (cilia). Arrows denote cilia located away from the ventricular surface, while arrowheads mark non-centrosomal Arl13b (dissociated ciliary remnants). Scale bar = 5 µm.

(B) Quantification of centrosomal versus non-centrosomal Arl13b in WT, Wdr62 −/− and Wdr62 −/−; Aspm +/− brains. Fisher’s exact test, ** p = 0.002 for WT vs. Wdr62 −/− and ** p = 0.009 for WT vs. Wdr62 −/−; Aspm +/−.

(C–D) Loss-of-function of Wdr62, Aspm or both severely disrupts apical complex proteins Pals1 and aPKCζ in a dose-dependent manner. From top to bottom: WT, Wdr62 +/−, Aspm −/−, Wdr62 +/−; Aspm −/− and Wdr62 −/− brains at E14.5 stained for (C) Pals1 and (D) aPKCζ to label the apical complex, and counterstained with DAPI. Scale bar = 50 µm.