ArticlePloS one2014
Hemizygous Le-Cre transgenic mice have severe eye abnormalities on some genetic backgrounds in the absence of LoxP sites.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 34 citations in OpenAlex.
- Glucocorticoid Receptor Signaling Is Critical for Mouse Corneal Development, Inhibition of Inflammatory Response, and Neovascularization of the Cornea.The American journal of pathology · 2024Article
- Review
- A tamoxifen-inducible Cre knock-in mouse for lens-specific gene manipulation.Experimental eye research · 2023Article
- Embryonic and early postnatal cranial bone volume and tissue mineral density values for C57BL/6J laboratory mice.Developmental dynamics : an official publication of the American Association of Anatomists · 2022Article
- Impaired GSH biosynthesis disrupts eye development, lens morphogenesis and PAX6 function.The ocular surface · 2021Article
- Pathogenic Role of PPARα Downregulation in Corneal Nerve Degeneration and Impaired Corneal Sensitivity in Diabetes.Diabetes · 2020Article
- Lens-specific conditional knockout of Msx2 in mice leads to ocular anterior segment dysgenesis via activation of a calcium signaling pathway.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- Considerations for the use of Cre recombinase for conditional gene deletion in the mouse lens.Human genomics · 2019Article
- The core planar cell polarity gene, Vangl2, maintains apical-basal organisation of the corneal epithelium.Journal of anatomy · 2019Article
- Epistasis between Pax6Gene therapy · 2018Article
- A conditional Pax6 depletion study with no morphological effect on the adult mouse corneal epithelium.BMC research notes · 2018Article
- Embryonic Surface Ectoderm-specific Mitofusin 2 Conditional Knockout Induces Congenital Cataracts in Mice.Scientific reports · 2018Article
- The L-type voltage-gated calcium channel CaLearning & memory (Cold Spring Harbor, N.Y.) · 2017Article
- Spatiotemporally Controlled Ablation of Klf5 Results in Dysregulated Epithelial Homeostasis in Adult Mouse Corneas.Investigative ophthalmology & visual science · 2017Article
- Genetic modifiers as relevant biological variables of eye disorders.Human molecular genetics · 2017Review
- miR-205 is a critical regulator of lacrimal gland development.Developmental biology · 2017Article
- Lens development requires DNMT1 but takes place normally in the absence of both DNMT3A and DNMT3B activity.Epigenetics · 2017Article
- Analysis of compound heterozygotes reveals that the mouse floxed Pax6 (tm1Ued) allele produces abnormal eye phenotypes.Transgenic research · 2016Article
- The core planar cell polarity gene,Royal Society open science · 2016Article
- FGFR and PTEN signaling interact during lens development to regulate cell survival.Developmental biology · 2016Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Eye phenotypes were investigated in Le-Cre(Tg/-); Pax6(fl/+) mice, which were expected to show tissue-specific reduction of Pax6 in surface ectoderm derivatives. To provide a better comparison with our previous studies of Pax6(+/-) eye phenotypes, hemizygous Le-Cre(Tg/-) and heterozygous Pax6(fl/+)mice were crossed onto the CBA/Ca genetic background. After the Le-Cre transgene had been backcrossed to CBA/Ca for seven generations, significant eye abnormalities occurred in some hemizygous Le-Cre(Tg/-); Pax6(+/+) controls (without a floxed Pax6(fl) allele) as well as experimental Le-Cre(Tg/-); Pax6(fl/+) mice. However, no abnormalities were seen in Le-Cre(-/-); Pax6(fl/+) or Le-Cre(-/-); Pax6(+/+) controls (without the Le-Cre transgene). The severity and frequency of the eye abnormalities in Le-Cre(Tg/-); Pax6(+/+) control mice diminished after backcrossing Le-Cre(Tg/-) mice to the original FVB/N strain for two generations, showing that the effect was reversible. This genetic background effect suggests that the eye abnormalities are a consequence of an interaction between the Le-Cre transgene and alleles of unknown modifier genes present in certain genetic backgrounds. The abnormalities were also ameliorated by introducing additional Pax6 gene copies on a CBA/Ca background, suggesting involvement of Pax6 depletion in Le-Cre(Tg/-); Pax6(+/+) mice rather than direct action of Cre recombinase on cryptic pseudo-loxP sites. One possibility is that expression of Cre recombinase from the Pax6-Le regulatory sequences in the Le-Cre transgene depletes cofactors required for endogenous Pax6 gene expression. Our observation that eye abnormalities can occur in hemizygous Le-Cre(Tg/-); Pax6(+/+) mice, in the absence of a floxed allele, demonstrates the importance of including all the relevant genetic controls in Cre-loxP experiments.
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