ArticleMolecular vision2012
Differences in corneal phenotypes between destrin mutants are due to allelic difference and modified by genetic background.
Article in Molecular vision, 2012. 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, 11 citations in OpenAlex.
- Bone morphogenetic protein 4 thermosensitive hydrogel inhibits corneal neovascularization by repairing corneal epithelial apical junctional complexes.Materials today. Bio · 2024Article
- How well do you know your mutation? Complex effects of genetic background on expressivity, complementation, and ordering of allelic effects.PLoS genetics · 2017Article
- Genetic modifiers as relevant biological variables of eye disorders.Human molecular genetics · 2017Review
- Length regulation of mechanosensitive stereocilia depends on very slow actin dynamics and filament-severing proteins.Nature communications · 2015Article
- Serum response factor: positive and negative regulation of an epithelial gene expression network in the destrin mutant cornea.Physiological genomics · 2014Article
- Genetic modification of corneal neovascularization in Dstn (corn1) mice.Mammalian genome : official journal of the International Mammalian Genome Society · 2013Article
- Changes in ADF/destrin expression in the development of hair cells following Atoh1-induced ectopic regeneration.Experimental and therapeutic medicine · 2013Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
purposeMutations in destrin (Dstn) cause corneal abnormalities in mice. A null mutation, Dstn(corn1), results in corneal epithelial hyperproliferation, inflammation, and neovascularization in the A.BY background (A.BY Dstn(corn1)). Homozygosity for a point mutation, Dstn(corn1-2J), results in mild thickening of the corneal epithelium but no corneal neovascularization in a C57BL/6 (B6) background (B6 Dstn(corn1-2J)). The goal of this study was to determine whether phenotypic differences are due to allelic differences between Dstn(corn1) and Dstn(corn1-2J), or are the result of genetic background effects.
methodsWe generated two congenic (Cg) mouse lines, B6.Cg-Dstn(corn1) and A.BY.Cg-Dstn(corn1-2J), to compare to the original A.BY Dstn(corn1) and B6 Dstn(corn1-2J) lines. We performed immunohistochemistry to assay F-actin accumulation, neovascularization, proliferation, and inflammation. By western blot analysis we tested the expression of serum response factor (SRF), a known regulator of the Dstn(corn1) phenotype.
resultsThe Dstn(corn1) mutation leads to neovascularization, hyperproliferation, and inflammation in the cornea of A.BY Dstn(corn1) as well as B6.Cg-Dstn(corn1) mice. We did not observe significant corneal neovascularization or hyperproliferation in either A.BY.Cg-Dstn(corn1-2J) or B6 Dstn(corn1-2J) mice. Actin accumulation, neovascularization, epithelial proliferation and inflammation in B6.Cg-Dstn(corn1) cornea are significantly reduced when compared to A.BY Dstn(corn1)cornea. SRF changes are consistent in Dstn(corn1) mutants, regardless of genetic background.
conclusionsDifferences in the abnormal phenotypes of Dstn mutants result from allelic differences between Dstn(corn1) and Dstn(corn1-2J) . Moreover, phenotypes of Dstn(corn1) mice are modified by genetic background, suggesting the existence of genetic modifiers. Protein analysis suggests that a genetic modifier affects phenotypic severity functionally downstream from or in a pathway independent from SRF. These data demonstrate that natural genetic variation affects phenotypic severity in Dstn(corn1) mice.
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Identifiers
22419854PMC3298451W1555879451What OpenQuestion holds
Registered trials
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