Analysis of aPKCλ and aPKCC reveals multiple and redundant functions during vertebrate retinogenesis

被引:39
作者
Cui, Shuang
Otten, Cecile
Rohr, Stefan
Abdelilah-Seyfried, Salim
Link, Brian A. [1 ]
机构
[1] Med Coll Wisconsin, Dept Cell Biol Neurobiol & Anat, Milwaukee, WI 53226 USA
[2] Max Delbruck Ctr Mol Med, D-13125 Berlin, Germany
关键词
neurogenesis; RPE; polarity; migration; ocular development; morphogenesis;
D O I
10.1016/j.mcn.2006.11.016
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Retinal lamination is known to depend on cell polarity and localized signaling. In vertebrates, atypical protein kinase C proteins, aPKC lambda/iota and aPKC zeta, 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 aPKCC 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. (c) 2006 Elsevier Inc. All rights reserved.
引用
收藏
页码:431 / 444
页数:14
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