ArticleThe British journal of ophthalmology2004
Mouse genetic corneal disease resulting from transgenic insertional mutagenesis.
Article in The British journal of ophthalmology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 3 citations in OpenAlex.
- Genetic modifiers as relevant biological variables of eye disorders.Human molecular genetics · 2017Review
- Enucleation for treating rodent ocular disease.Journal of the American Association for Laboratory Animal Science : JAALAS · 2015Article
- The PPCD1 mouse: characterization of a mouse model for posterior polymorphous corneal dystrophy and identification of a candidate gene.PloS one · 2010Article
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4 authors at 1 institution in 1 country.
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Abstract
BACKGROUND/
aimsTo report the generation of a new mouse model for a genetically determined corneal abnormality that occurred in transgenesis experiments.
methodsTransgenic mice expressing mutant forms of Rab27a, a GTPase that has been implicated in the pathogenesis of choroideremia, were generated.
resultsOnly one transgenic line (T27aT15) exhibited an unexpected eye phenotype. T27aT15 mice developed corneal opacities, usually unilateral, and cataracts, resulting in some cases in phthisical eyes. Histologically, the corneal stroma was thickened and vacuolated, and both epithelium and endothelium were thinned. The posterior segment of the eye was also affected with abnormal pigmentation, vessel narrowing, and abnormal leakage of dye upon angiography but was histologically normal.
conclusionEye abnormality in T27aT15 mice results from random insertional mutagenesis of the transgene as it was only observed in one line. The corneal lesion observed in T27aT15 mice most closely resembles posterior polymorphous corneal dystrophy and might result from the disruption of the equivalent mouse locus.
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