PUBLICATION
The role of mip in the development of lens in zebrafish
- Authors
- He, M., Zhou, G., Lin, Q., Zhou, N.
- ID
- ZDB-PUB-230628-49
- Date
- 2023
- Source
- Gene expression patterns : GEP 49: 119330 (Journal)
- Registered Authors
- Keywords
- Cas9, Knock out, Lens, Zebrafish, mip
- MeSH Terms
-
- Cataract*/genetics
- Cataract*/metabolism
- Cataract*/pathology
- Lens, Crystalline*/metabolism
- Lens, Crystalline*/pathology
- Animals
- Zebrafish/genetics
- Zebrafish/metabolism
- Aquaporins*/metabolism
- Eye Proteins/genetics
- Eye Proteins/metabolism
- PubMed
- 37369320 Full text @ Gene Expr. Patterns
Citation
He, M., Zhou, G., Lin, Q., Zhou, N. (2023) The role of mip in the development of lens in zebrafish. Gene expression patterns : GEP. 49:119330.
Abstract
Major intrinsic protein (MIP) functions as a water channel and a cell-junction molecule in the vertebrate eye lens. The pathogenic mechanism behind the loss of MIP function in the lens, which leads to degraded optical quality and cataract formation, is still unclear. In this study, a zebrafish model with the mipb mutant was produced. The expression of mipb mRNA and protein was dramatically reduced in the mutant. Immunological analysis reveals that loss function of mip leads to the diffuse distribution of ZL-1 in the mutant lens. Furthermore, in situ hybridization reveals that mip knockout results in a decrease in the transcripts of beaded filament structural protein 2 (Bfsp2) in the lens. Histology study shows that lens fibers in the mutants are less uniform in shape and the fiber arrangement is disrupted. The presented data provides evidence for the essential role of mipb in the development of lens fibers. The absence of mipb during lens formation is likely to result in aberrant lens fiber formation and impaired lens function.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping