Generation and characterization of Aldh3-Cre transgenic mice as a tool for conditional gene deletion in postnatal cornea
Jazyk angličtina Země Anglie, Velká Británie Médium electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
32493941
PubMed Central
PMC7270111
DOI
10.1038/s41598-020-65878-1
PII: 10.1038/s41598-020-65878-1
Knihovny.cz E-zdroje
- MeSH
- aldehyddehydrogenasa genetika MeSH
- alely MeSH
- delece genu MeSH
- epitelové buňky fyziologie MeSH
- genový targeting metody MeSH
- integrasy genetika MeSH
- konjunktiva fyziologie MeSH
- myši transgenní genetika fyziologie MeSH
- myši MeSH
- rohovka fyziologie MeSH
- zvířata MeSH
- Check Tag
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- aldehyddehydrogenasa MeSH
- Aldh3a1protein, mouse MeSH Prohlížeč
- Cre recombinase MeSH Prohlížeč
- integrasy MeSH
Conditional gene targeting in mice by means of Cre-loxP strategy represents a powerful approach to study mammalian gene function. This approach is however dependent on the availability of suitable strains of mice with a tissue or time restricted activity of the Cre recombinase. Here we describe Aldh3-Cre transgenic mice as a useful tool to conditionally delete genes in cornea, a specialized transparent tissue found on the anterior-most part of the eye, which acts as a protective barrier and contributes to the refractive power. Using a set of floxed alleles we demonstrate high Aldh3-Cre activity in corneal epithelial cells, corneal stroma and conjunctival epithelial cells at postnatal stages. Aldh3-Cre will thus be particularly beneficial for functional analysis of genes which are vital for postnatal development of cornea and conjunctiva.
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Zieske JD. Corneal development associated with eyelid opening. Int. J. Dev. Biol. 2004;48:903–911. doi: 10.1387/ijdb.041860jz. PubMed DOI
Hay ED. Development of the vertebrate cornea. Int. Rev. Cytol. 1980;63:263–322. doi: 10.1016/s0074-7696(08)61760-x. PubMed DOI
Pei YF, Rhodin JA. Electron microscopic study of the development of the mouse corneal epithelium. Invest. Ophthalmol. 1971;10:811–825. PubMed
Haustein J. On the ultrastructure of the developing and adult mouse corneal stroma. Anat. Embryol. 1983;168:291–305. doi: 10.1007/bf00315823. PubMed DOI
Collinson JM, et al. Clonal analysis of patterns of growth, stem cell activity, and cell movement during the development and maintenance of the murine corneal epithelium. Dev. Dyn. 2002;224:432–440. doi: 10.1002/dvdy.10124. PubMed DOI
Nagasaki T, Zhao J. Centripetal movement of corneal epithelial cells in the normal adult mouse. Invest. Ophthalmol. Vis. Sci. 2003;44:558–566. doi: 10.1167/iovs.02-0705. PubMed DOI
Cotsarelis G, Cheng SZ, Dong G, Sun TT, Lavker RM. Existence of slow-cycling limbal epithelial basal cells that can be preferentially stimulated to proliferate: implications on epithelial stem cells. Cell. 1989;57:201–209. doi: 10.1016/0092-8674(89)90958-6. PubMed DOI
Klintworth GK. The molecular genetics of the corneal dystrophies–current status. Front. Biosci. 2003;8:d687–713. doi: 10.2741/1018. PubMed DOI
Hogan BL, et al. Small eyes (Sey): a homozygous lethal mutation on chromosome 2 which affects the differentiation of both lens and nasal placodes in the mouse. J. Embryol. Exp. Morphol. 1986;97:95–110. PubMed
Hill RE, et al. Mouse small eye results from mutations in a paired-like homeobox-containing gene. Nature. 1991;354:522–525. doi: 10.1038/354522a0. PubMed DOI
Gu H, Marth JD, Orban PC, Mossmann H, Rajewsky K. Deletion of a DNA polymerase beta gene segment in T cells using cell type-specific gene targeting. Science. 1994;265:103–106. doi: 10.1126/science.8016642. PubMed DOI
Gu H, Zou YR, Rajewsky K. Independent control of immunoglobulin switch recombination at individual switch regions evidenced through Cre-loxP-mediated gene targeting. Cell. 1993;73:1155–1164. doi: 10.1016/0092-8674(93)90644-6. PubMed DOI
Swamynathan SK, et al. Conditional deletion of the mouse Klf4 gene results in corneal epithelial fragility, stromal edema, and loss of conjunctival goblet cells. Mol. Cell Biol. 2007;27:182–194. doi: 10.1128/MCB.00846-06. PubMed DOI PMC
Lu H, Lu Q, Zheng Y, Li Q. Notch signaling promotes the corneal epithelium wound healing. Mol. Vis. 2012;18:403–411. PubMed PMC
Kokado M, et al. Lack of plakoglobin impairs integrity and wound healing in corneal epithelium in mice. Lab. Invest. 2018;98:1375–1383. doi: 10.1038/s41374-018-0082-z. PubMed DOI
Tanifuji-Terai N, Terai K, Hayashi Y, Chikama T, Kao WW. Expression of keratin 12 and maturation of corneal epithelium during development and postnatal growth. Invest. Ophthalmol. Vis. Sci. 2006;47:545–551. doi: 10.1167/iovs.05-1182. PubMed DOI
Weng DY, et al. Promiscuous recombination of LoxP alleles during gametogenesis in cornea Cre driver mice. Mol. Vis. 2008;14:562–571. PubMed PMC
Joo JH, Kim YH, Dunn NW, Sugrue SP. Disruption of mouse corneal epithelial differentiation by conditional inactivation of pnn. Invest. Ophthalmol. Vis. Sci. 2010;51:1927–1934. doi: 10.1167/iovs.09-4591. PubMed DOI PMC
Abedinia M, Pain T, Algar EM, Holmes RS. Bovine corneal aldehyde dehydrogenase: the major soluble corneal protein with a possible dual protective role for the eye. Exp. Eye Res. 1990;51:419–426. doi: 10.1016/0014-4835(90)90154-m. PubMed DOI
Pappa A, Sophos NA, Vasiliou V. Corneal and stomach expression of aldehyde dehydrogenases: from fish to mammals. Chem. Biol. Interact. 2001;130-132:181–191. doi: 10.1016/s0009-2797(00)00233-7. PubMed DOI
Chen Y, Thompson DC, Koppaka V, Jester JV, Vasiliou V. Ocular aldehyde dehydrogenases: protection against ultraviolet damage and maintenance of transparency for vision. Prog. Retin. Eye Res. 2013;33:28–39. doi: 10.1016/j.preteyeres.2012.10.001. PubMed DOI PMC
Davis J, Davis D, Norman B, Piatigorsky J. Gene expression of the mouse corneal crystallin Aldh3a1: activation by Pax6, Oct1, and p300. Invest. Ophthalmol. Vis. Sci. 2008;49:1814–1826. doi: 10.1167/iovs.07-1057. PubMed DOI
Soriano P. Generalized lacZ expression with the ROSA26 Cre reporter strain. Nat. Genet. 1999;21:70–71. doi: 10.1038/5007. PubMed DOI
Kays WT, Piatigorsky J. Aldehyde dehydrogenase class 3 expression: identification of a cornea-preferred gene promoter in transgenic mice. Proc. Natl Acad. Sci. USA. 1997;94:13594–13599. doi: 10.1073/pnas.94.25.13594. PubMed DOI PMC
Harada N, et al. Intestinal polyposis in mice with a dominant stable mutation of the beta-catenin gene. EMBO J. 1999;18:5931–5942. doi: 10.1093/emboj/18.21.5931. PubMed DOI PMC
Zhang Y, et al. Aberrant expression of a beta-catenin gain-of-function mutant induces hyperplastic transformation in the mouse cornea. J. Cell Sci. 2010;123:1285–1294. doi: 10.1242/jcs.063321. PubMed DOI PMC
Zhang L, et al. Aberrant expression of a stabilized beta-catenin mutant in keratocytes inhibits mouse corneal epithelial stratification. Sci. Rep. 2019;9:1919. doi: 10.1038/s41598-018-36392-2. PubMed DOI PMC
Brault V, et al. Inactivation of the beta-catenin gene by Wnt1-Cre-mediated deletion results in dramatic brain malformation and failure of craniofacial development. Development. 2001;128:1253–1264. PubMed
Zhang Y, et al. Wnt/beta-catenin signaling modulates corneal epithelium stratification via inhibition of Bmp4 during mouse development. Development. 2015;142:3383–3393. doi: 10.1242/dev.125393. PubMed DOI PMC
Norman B, Davis J, Piatigorsky J. Postnatal gene expression in the normal mouse cornea by SAGE. Invest. Ophthalmol. Vis. Sci. 2004;45:429–440. doi: 10.1167/iovs.03-0449. PubMed DOI
Lee EC, et al. A highly efficient Escherichia coli-based chromosome engineering system adapted for recombinogenic targeting and subcloning of BAC DNA. Genomics. 2001;73:56–65. doi: 10.1006/geno.2000.6451. PubMed DOI