ArticleInvestigative ophthalmology & visual science2011
Ectopic proliferation contributes to retinal dysplasia in the juvenile zebrafish patched2 mutant eye.
Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 4 citations in OpenAlex.
- Roles of sonic hedgehog signaling in retinal patterning and neurogenesis during mammalian eye development.Development (Cambridge, England) · 2026Article
- Retinal Stem Cell 'Retirement Plans': Growth, Regulation and Species Adaptations in the Retinal Ciliary Marginal Zone.International journal of molecular sciences · 2021Review
- Sox4 regulates choroid fissure closure by limiting Hedgehog signaling during ocular morphogenesis.Developmental biology · 2015Article
- Development of the Vertebrate Eye and Retina.Progress in molecular biology and translational science · 2015Review
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2 authors at 1 institution in 1 country.
Funding
Abstract
purposePatched is a well-studied tumor suppressor and negative regulator of the Hedgehog (Hh) pathway. Earlier work in this laboratory has shown that embryonic zebrafish patched2 (ptc2) mutant retinas possess an expanded ciliary marginal zone (CMZ) and phenotypes similar to those in human patients with basal cell naevus syndrome (BCNS), a congenital disorder linked to mutations in the human PTCH gene. This study extends the analysis of retinal structure and homeostasis in ptc2-/- mutants to juvenile stages, to determine whether Patched 2 function is essential in the postembryonic eye.
methodsHistologic, immunohistochemical, and molecular analyses were used to characterize retinal defects in the 6-week-old juvenile ptc2-/- retina.
resultsJuvenile ptc2-/- mutants exhibited peripheral retinal dysplasias that included the presence of ectopic neuronal clusters in the inner nuclear layer (INL) and regions of disrupted retinal lamination. Retinal dysplasias were locally associated with ectopic proliferation. BrdU/EdU labeling and immunohistochemistry assays demonstrated that a population of ectopically proliferating cells gave rise to the ectopic neuronal clusters in the INL of ptc2-/- mutants and that this contributed to retinal dysplasia in the mutant eye.
conclusionsThese results demonstrate a direct link between overproliferation and retinal dysplasia in the ptc2-/- juvenile retina and establish ectopic proliferation as the likely cellular underpinning of retinal dysplasia in juvenile ptc2-/- mutants.
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