Fig. 8.

Working model for the role of PCP in ependymal polarity. Apical surface during transition from RG (P1) to ependymal cells (P21). In WT, the BB of the primary cilium (red dot) is off-centered. An MT network (green) extending from the centrosome to the cortex generates a biased distribution of PCP proteins (gray bars, putatively Fzd3; green bars, Vangl2). At P5, BBs of multicilia (dots) appear widespread and randomly oriented. Concomitant to BB clustering, actin (black) and MT (green) meshworks appear underneath the surface (gray area). MTs (green dashed arrows) connect patches and the cell cortex. In Celsr1^−/−, the primary cilium localization and PCP protein distribution are impaired. The patch–cortex MT interactions occur, but the altered distribution of proteins lead to abnormal positioning and orientation of the BB patch. In contrast, actin and MT networks located in the patch area are unaffected, which results in a normal organization of the BB array. In Celsr2^−/−and Celsr3^cKO, the primary cilium is correctly positioned, and it correlates with a normal partition of PCP proteins. Patch–cortex MT interactions are preserved, and patches are correctly positioned and orientated. At the level of individual BB patches, the intrapatch cytoskeleton and the shape of BB array are altered.