ArticleDevelopmental dynamics : an official publication of the American Association of Anatomists2007
Zebrafish dou yan mutation causes patterning defects and extensive cell death in the retina.
Article in Developmental dynamics : an official publication of the American Association of Anatomists, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Collective behaviour in vertebrates: a sensory perspective.Royal Society open science · 2016Article
- Characterization of zebrafish Pax1b and Pax9 in fin bud development.BioMed research international · 2014Article
- Toward a better understanding of human eye disease insights from the zebrafish, Danio rerio.Progress in molecular biology and translational science · 2011Review
- Transplantation of GFP-expressing blastomeres for live imaging of retinal and brain development in chimeric zebrafish embryos.Journal of visualized experiments : JoVE · 2010Article
- Expression of a 12-kb promoter element derived from the zebrafish enolase-2 gene in the zebrafish visual system.Neuroscience letters · 2009Article
- Intact retinal pigment epithelium maintained by Nok is essential for retinal epithelial polarity and cellular patterning in zebrafish.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Chemical genetic effects of Sargassum wightii during embryonic development in zebrafish.Indian journal of pharmacologyArticle
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Abstract
The size of an organ is largely determined by the number of cells it contains, which in turn is regulated by two opposing processes, cell proliferation and cell death, however, it is generally not clear how cell proliferation and cell death are coordinated during development. Here, we characterize the zebrafish dou yan(mi234) mutation that results in a dramatic reduction of retinal size and a disruption of retinal differentiation and lamination. The retinal size reduction is caused by increased retinal cell death in a non-cell-autonomous manner during early development. The phenotypic defect in dou yan(mi234) arises coincident with the onset of retinal neurogenesis and differentiation. Interestingly, unlike many other small eye mutations, the mutation does not increase the level of cell death in the brain, suggesting that the brain and retina use different mechanisms to maintain cell survival. Identification and further study of the dou yan gene will enhance our understanding of the molecular mechanisms regulating retinal cellular homeostasis, i.e., the balance between cell proliferation and cell death.
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