期刊
MOLECULAR AND CELLULAR NEUROSCIENCE
卷 34, 期 3, 页码 431-444出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mcn.2006.11.016
关键词
neurogenesis; RPE; polarity; migration; ocular development; morphogenesis
资金
- NEI NIH HHS [R01 EY014167-04, R01 EY014167, R01 EY014167-02, R01 EY014167-01A1S1, R01 EY014167-01A1, R01 EY014167-03, R01EY01467, R01 EY014167-05A1] Funding Source: Medline
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.
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