ArticleScientific reports2016
Melanosomes in pigmented epithelia maintain eye lens transparency during zebrafish embryonic development.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 11 citations in OpenAlex.
- Zebrafish in dermatology: a comprehensive review of their role in investigating abnormal skin pigmentation mechanisms.Frontiers in physiology · 2023Review
- Some Aspects of Development and Histological Structure of the Visual System of Nothobranchius Guentheri.Animals : an open access journal from MDPI · 2021Article
- Proteasome subunit PSMC3 variants cause neurosensory syndrome combining deafness and cataract due to proteotoxic stress.EMBO molecular medicine · 2020Article
- Pax6 organizes the anterior eye segment by guiding two distinct neural crest waves.PLoS genetics · 2020Article
- Imaging cell morphology and physiology using X-rays.Biochemical Society transactions · 2019Review
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Authors and funding
15 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
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