PUBLICATION

Melanosomes in pigmented epithelia maintain eye lens transparency during zebrafish embryonic development

Authors
Takamiya, M., Xu, F., Suhonen, H., Gourain, V., Yang, L., Ho, N.Y., Helfen, L., Schröck, A., Etard, C., Grabher, C., Rastegar, S., Schlunck, G., Reinhard, T., Baumbach, T., Strähle, U.
ID
ZDB-PUB-160505-5
Date
2016
Source
Scientific Reports   6: 25046 (Journal)
Registered Authors
Etard, Christelle, Gourain, Victor, Grabher, Clemens, Ho, Nga Yu, Rastegar, Sepand, Strähle, Uwe, Takamiya, Masanari, Yang, Lixin
Keywords
Embryonic induction, Mechanisms of disease, X-ray tomography
MeSH Terms
  • Animals
  • Cataract/prevention & control
  • Embryonic Development*
  • Lens, Crystalline/chemistry
  • Lens, Crystalline/embryology*
  • Lens, Crystalline/physiology*
  • Melanosomes/metabolism*
  • Oxidative Stress
  • Pigments, Biological/metabolism
  • Spectrometry, X-Ray Emission
  • Trace Elements/analysis
  • Zebrafish/embryology*
PubMed
27141993 Full text @ Sci. Rep.
Abstract
Altered levels of trace elements are associated with increased oxidative stress that is eventually responsible for pathologic conditions. Oxidative stress has been proposed to be involved in eye diseases, including cataract formation. We visualized the distribution of metals and other trace elements in the eye of zebrafish embryos by micro X-ray fluorescence (μ-XRF) imaging. Many elements showed highest accumulation in the retinal pigment epithelium (RPE) of the zebrafish embryo. Knockdown of the zebrafish brown locus homologues tyrp1a/b eliminated accumulation of these elements in the RPE, indicating that they are bound by mature melanosomes. Furthermore, albino (slc45a2) mutants, which completely lack melanosomes, developed abnormal lens reflections similar to the congenital cataract caused by mutation of the myosin chaperon Unc45b, and an in situ spin trapping assay revealed increased oxidative stress in the lens of albino mutants. Finally transplanting a wildtype lens into an albino mutant background resulted in cataract formation. These data suggest that melanosomes in pigment epithelial cells protect the lens from oxidative stress during embryonic development, likely by buffering trace elements.
Genes / Markers
Figures
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes