PUBLICATION
Zebrafish Mosaic Eyes Is a Novel FERM Protein Required for Retinal Lamination and Retinal Pigmented Epithelial Tight Junction Formation
- Authors
- Jensen, A.M., and Westerfield, M.
- ID
- ZDB-PUB-040416-3
- Date
- 2004
- Source
- Current biology : CB 14(8): 711-717 (Journal)
- Registered Authors
- Jensen, Abigail, Westerfield, Monte
- Keywords
- none
- MeSH Terms
-
- Amino Acid Sequence
- Animals
- Cell Polarity/physiology*
- Cluster Analysis
- Eye Proteins/genetics*
- Eye Proteins/physiology
- Gene Expression
- Immunohistochemistry
- In Situ Hybridization
- Membrane Proteins
- Molecular Sequence Data
- Oligodeoxyribonucleotides, Antisense
- Phylogeny*
- Pigment Epithelium of Eye/cytology*
- Protein Structure, Tertiary
- Retina/cytology*
- Retina/physiology
- Sequence Alignment
- Sequence Analysis, DNA
- Tight Junctions/physiology*
- Zebrafish/physiology*
- Zebrafish Proteins/genetics*
- Zebrafish Proteins/physiology
- PubMed
- 15084287 Full text @ Curr. Biol.
Citation
Jensen, A.M., and Westerfield, M. (2004) Zebrafish Mosaic Eyes Is a Novel FERM Protein Required for Retinal Lamination and Retinal Pigmented Epithelial Tight Junction Formation. Current biology : CB. 14(8):711-717.
Abstract
Polarization is a common feature of many types of cells, and we are beginning to understand how cells become polarized. The role of cell polarity in development and tissue morphogenesis, however, is much less well understood. Our previous analysis of the mosaic eyes (moe) mutations revealed that moe is required for retinal lamination and also suggested that zebrafish moe function is required in the retinal pigmented epithelium (RPE) for the proper localization of adjacent retinal cell divisions at the apical neuroepithelial surface. To understand the function of moe in the RPE, we cloned the moe locus and show that it encodes a novel FERM (for 4.1 protein, ezrin, radixin, moesin) domain-containing protein. Expression of moe in the eye, kidney, and brain reflects phenotypes found in moe(-) mutants, including RPE and retinal lamination defects, edema, and small or absent brain ventricles. We show that moe function is required for tight junction formation in the RPE. We suggest that moe may be a necessary component of the crumbs pathway that regulates apical cell polarity and also may play a role in photoreceptor morphogenesis.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping