Genetic analysis of photoreceptor cell development in the zebrafish retina.
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.
Doerre
Geoffrey
G
Department of Ophthalmology, Harvard Medical School, 243 Charles Street, Boston, MA 02114, USA.
Malicki
Jarema
J
D000818:Animals; D002450:Cell Communication / Q000235:genetics; D016923:Cell Death / Q000235:genetics; D008854:Microscopy, Electron; D009030:Mosaicism / Q000235:genetics; D009154:Mutation; D010641:Phenotype; D020419:Photoreceptor Cells, Vertebrate / Q000166:cytology* / Q000378:metabolism; D012160:Retina / Q000166:cytology / Q000254:growth & development; D012168:Retinal Pigments / Q000378:metabolism; D015027:Zebrafish / Q000235:genetics* / Q000254:growth & development* / Q000378:metabolism
D012168:Retinal Pigments