期刊
MECHANISMS OF DEVELOPMENT
卷 110, 期 1-2, 页码 125-138出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/S0925-4773(01)00571-8
关键词
eye; retina; photoreceptor; cell-nonautonomy; cell-cell interaction; zebrafish; mutant
资金
- NATIONAL EYE INSTITUTE [R01EY011882, T32EY007145] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [T32AG000222] Funding Source: NIH RePORTER
- NEI NIH HHS [R01 EY11882-01A1, T32-EY07145] Funding Source: Medline
- NIA NIH HHS [T32-AG00222] Funding Source: Medline
To gain insight into the genetic mechanisms of photoreceptor development, we analyzed a collection of zebrafish mutations characterized by early photoreceptor cell loss. The mutant defects impair outer segment formation and are accompanied by an abnormal distribution of visual pigments. Rods and different cone types display defects of similar severity suggesting that genetic pathways common to all photoreceptors are affected. To investigate whether these phenotypes involve cell-cell interaction defects, we analyzed genetically mosaic animals, Interaction of niezerka photoreceptors with wild-type tissues improves the survival of mutant cells and restores their elongated morphology. In contrast, cells carrying mutations in the loci brudas, elipsa, fleer, and oval retain their defective phenotypes in a wild-type environment indicating cell-autonomy. These experiments identify distinct phenotypic categories of photoreceptor mutants and indicate that zebrafish photoreceptor defects involve both cell-autonomous and cell-nonautonomous mechanisms. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
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