Analysis of aPKClambda and aPKCzeta reveals multiple and redundant functions during vertebrate retinogenesis.

Retinal lamination is known to depend on cell polarity and localized signaling. In vertebrates, atypical protein kinase C proteins, aPKClambda/iota and aPKCzeta, are essential for apical-basal cell polarity. However, it is not known to what extent functional redundancy has precluded a comprehensive functional characterization of aPKC signaling during vertebrate retinogenesis. Here, we show that aPKCs lambda and zeta are functionally redundant for multiple aspects of retinogenesis including mitotic division location and orientation, cell-type positioning, and retinal pigment epithelial (RPE) and photoreceptor cell morphogenesis. Genetic mosaic analyses demonstrate a cell-autonomous requirement of aPKCs for RPE and photoreceptor development, and a cell-non-cell-autonomous function that is intrinsic to the neural retina for cell-type positioning. Our observations uncover a previously unappreciated involvement of aPKCzeta during zebrafish retinogenesis and suggest that aPKC signaling primes the retinal environment for appropriate cell migration of post-mitotic progenitor cells but is not essential for correct cell-type specification.