A minimal Ksp-cadherin promoter linked to a green fluorescent protein reporter gene exhibits tissue-specific expression in the developing kidney and genitourinary tract
- PMID: 12089378
- DOI: 10.1097/01.asn.0000016443.50138.cd
A minimal Ksp-cadherin promoter linked to a green fluorescent protein reporter gene exhibits tissue-specific expression in the developing kidney and genitourinary tract
Abstract
Ksp-cadherin is a unique, tissue-specific member of the cadherin family of cell adhesion molecules that is expressed exclusively in tubular epithelial cells in the kidney and developing genitourinary (GU) tract. Transgenic mice carrying 3425 bp of the Ksp-cadherin 5' flanking region linked to a lacZ reporter gene express beta-galactosidase exclusively in the kidney, although the expression pattern is incomplete (Am J Physiol 277: F599-F610, 1999). To further define the region that mediates tissue-specific expression, transgenic mice carrying 1341 bp or 324 bp of the 5' flanking region linked to a green fluorescent protein (GFP) reporter gene were produced. Transgenic mice carrying 1341 bp of the 5' flanking region expressed GFP in all embryonic tissues that endogenously express Ksp-cadherin, including the ureteric bud, Wolffian duct, Müllerian duct, and developing tubules in the mesonephros and metanephros. In the adult kidney, GFP was highly expressed in thick ascending limbs of Henle's loops and collecting ducts and weakly expressed in proximal tubules and Bowman's capsules. Transgenic mice carrying 324 bp of the 5' flanking region exhibited expression exclusively in tubular epithelial cells in the developing kidney and GU tract. Immunoblot analysis showed that the expression of GFP was restricted to the kidney in adult mice. Taken together, these results demonstrate that 324 bp of the Ksp-cadherin 5' flanking region is sufficient to direct epithelial-specific expression in the developing kidney and GU tract. Transgenic mice that express GFP in the mesonephros, metanephros, ureteric bud, and sex ducts may be useful for cell lineage studies.
Similar articles
-
Epithelial-specific Cre/lox recombination in the developing kidney and genitourinary tract.J Am Soc Nephrol. 2002 Jul;13(7):1837-46. doi: 10.1097/01.asn.0000016444.90348.50. J Am Soc Nephrol. 2002. PMID: 12089379
-
Ksp-cadherin gene promoter. II. Kidney-specific activity in transgenic mice.Am J Physiol. 1999 Oct;277(4):F599-610. doi: 10.1152/ajprenal.1999.277.4.F599. Am J Physiol. 1999. PMID: 10516285
-
Ksp-cadherin gene promoter. I. Characterization and renal epithelial cell-specific activity.Am J Physiol. 1999 Oct;277(4):F587-98. doi: 10.1152/ajprenal.1999.277.4.F587. Am J Physiol. 1999. PMID: 10516284
-
Following the expression of a kidney-specific gene from early development to adulthood.Nephron Exp Nephrol. 2003;94(1):e1-6. doi: 10.1159/000070812. Nephron Exp Nephrol. 2003. PMID: 12806181 Review.
-
Essential roles of Sall1 in kidney development.Kidney Int. 2005 Nov;68(5):1948-50. doi: 10.1111/j.1523-1755.2005.00626.x. Kidney Int. 2005. PMID: 16221172 Review.
Cited by
-
Urothelial Defects from Targeted Inactivation of Exocyst Sec10 in Mice Cause Ureteropelvic Junction Obstructions.PLoS One. 2015 Jun 5;10(6):e0129346. doi: 10.1371/journal.pone.0129346. eCollection 2015. PLoS One. 2015. PMID: 26046524 Free PMC article.
-
Loss of cilia suppresses cyst growth in genetic models of autosomal dominant polycystic kidney disease.Nat Genet. 2013 Sep;45(9):1004-12. doi: 10.1038/ng.2715. Epub 2013 Jul 28. Nat Genet. 2013. PMID: 23892607 Free PMC article.
-
Comparing the Bbs10 complete knockout phenotype with a specific renal epithelial knockout one highlights the link between renal defects and systemic inactivation in mice.Cilia. 2015 Aug 13;4:10. doi: 10.1186/s13630-015-0019-8. eCollection 2015. Cilia. 2015. PMID: 26273430 Free PMC article.
-
Inactivation of Invs/Nphp2 in renal epithelial cells drives infantile nephronophthisis like phenotypes in mouse.Elife. 2023 Mar 15;12:e82395. doi: 10.7554/eLife.82395. Elife. 2023. PMID: 36920028 Free PMC article.
-
Rrm2b deletion causes mitochondrial metabolic defects in renal tubules.Sci Rep. 2019 Sep 13;9(1):13238. doi: 10.1038/s41598-019-49663-3. Sci Rep. 2019. PMID: 31519977 Free PMC article.
Publication types
MeSH terms
Substances
Grants and funding
LinkOut - more resources
Full Text Sources
Other Literature Sources
