Premium
Transgenic mice expressing tamoxifen‐inducible Cre for somatic gene modification in renal epithelial cells
Author(s) -
Lantingavan Leeuwen Irma S.,
Leonhard Wouter N.,
van de Wal Annemieke,
Breuning Martijn H.,
Verbeek Sjef,
de Heer Emile,
Peters Dorien J.M.
Publication year - 2006
Publication title -
genesis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.093
H-Index - 110
eISSN - 1526-968X
pISSN - 1526-954X
DOI - 10.1002/dvg.20207
Subject(s) - somatic cell , transgene , genetically modified mouse , tamoxifen , biology , gene , genetically modified organism , microbiology and biotechnology , cancer research , genetics , cancer , breast cancer
Gene inactivation often leads to an embryonic‐lethal phenotype. In focal diseases like renal cell carcinomas and polycystic kidney disease, somatic gene inactivation in subsets of cells is likely to occur at later stages. We generated a transgenic mouse line with an inducible form of Cre recombinase for conditional gene modifications in kidney epithelial cells. To this end a 1.4‐kb promoter fragment of the kidney‐specific cadherin gene (KspCad) was cloned upstream of a tamoxifen‐inducible Cre recombinase (CreER T2 ) encoding sequence. Expression and activity of Cre was evaluated using reverse transcriptase polymerase chain reaction (RT‐PCR) analysis and by crossbreeding to Z/EG reporter mice. One KspCad‐CreER T2 line showed kidney‐specific Cre expression and mediated recombination upon tamoxifen treatment in Z/EG reporter mice. No reporter gene expression was detected in untreated animals or in extrarenal tissues upon treatment. Within the kidneys, enhanced green fluorescent protein (EGFP) fluorescence was observed in epithelial cells in several nephronic segments. In addition, the system successfully recombined a floxed Pkd1 gene. genesis 44:225–232, 2006. © 2006 Wiley‐Liss, Inc.