ArticleExperimental eye research2013
Loss of the small heat shock protein αA-crystallin does not lead to detectable defects in early zebrafish lens development.
Article in Experimental eye research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Contributions of aquatic organisms to understanding the vertebrate ocular lens.Frontiers in ophthalmology · 2026Review
- Impact of α-crystallin protein loss on zebrafish lens development.Experimental eye research · 2023Article
- Single cell transcriptomics of the developing zebrafish lens and identification of putative controllers of lens development.Experimental eye research · 2021Article
- Why does the zebrafish cloche mutant develop lens cataract?PloS one · 2019Article
- Transgenic zebrafish models reveal distinct molecular mechanisms for cataract-linked αA-crystallin mutants.PloS one · 2018Article
- Transient cerebellar alterations during development prior to obvious motor phenotype in a mouse model of spinocerebellar ataxia type 6.The Journal of physiology · 2017Article
- Abnormal retinal development in Cloche mutant zebrafish.Developmental dynamics : an official publication of the American Association of Anatomists · 2015Article
- A conserved role of αA-crystallin in the development of the zebrafish embryonic lens.Experimental eye research · 2015Article
- NMDA glutamate receptor NR1, NR2A and NR2B expression and NR2B Tyr-1472 phosphorylation in the lens.Neurochemical research · 2014Article
- The role of a lens survival pathway including sox2 and αA-crystallin in the evolution of cavefish eye degeneration.EvoDevo · 2014Article
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Alpha crystallins are small heat shock proteins essential to normal ocular lens function. They also help maintain homeostasis in many non-ocular vertebrate tissues and their expression levels change in multiple diseases of the nervous and cardiovascular system and during cancer. The specific roles that α-crystallins may play in eye development are unclear. Studies with knockout mice suggested that only one of the two mammalian α-crystallins is required for normal early lens development. However, studies in two fish species suggested that reduction of αA-crystallin alone could inhibit normal fiber cell differentiation, cause cataract and contribute to lens degeneration. In this study we used synthetic antisense morpholino oligomers to suppress the expression of zebrafish αA-crystallin to directly test the hypothesis that, unlike mammals, the zebrafish requires αA-crystallin for normal early lens development. Despite the reduction of zebrafish αA-crystallin protein to undetectable levels by western analysis through 4 days of development we found no changes in fiber cell differentiation, lens morphology or transparency. In contrast, suppression of AQP0a expression, previously shown to cause lens cataract, produced irregularly shaped lenses, delay in fiber cell differentiation and lens opacities detectable by confocal microscopy. The normal development observed in αA-crystallin deficient zebrafish embryos may reflect similarly non-essential roles for this protein in the early stages of both zebrafish and mammalian lens development. This finding has ramifications for a growing number of researchers taking advantage of the zebrafish's transparent external embryos to study vertebrate eye development. Our demonstration that lens cataracts can be visualized in three-dimensions by confocal microscopy in a living zebrafish provides a new tool for studying the causes, development and prevention of lens opacities.
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