This article is a US Government work and, as such, is in the public domain in the United States of America.
Generation of a transgenic mouse model with chondrocyte-specific and tamoxifen-inducible expression of Cre recombinase†
Article first published online: 8 JAN 2007
Published 2007 Wiley-Liss, Inc.
Volume 45, Issue 1, pages 44–50, January 2007
How to Cite
Chen, M., Lichtler, A. C., Sheu, T.-J., Xie, C., Zhang, X., O'Keefe, R. J. and Chen, D. (2007), Generation of a transgenic mouse model with chondrocyte-specific and tamoxifen-inducible expression of Cre recombinase. Genesis, 45: 44–50. doi: 10.1002/dvg.20261
- Issue published online: 10 JAN 2007
- Article first published online: 8 JAN 2007
- Manuscript Accepted: 14 NOV 2006
- Manuscript Received: 10 OCT 2006
- National Institute of Health. Grant Numbers: R01 AR051189, K02 AR052411
- Cre-mediated recombination;
- conditional knockout;
- X-Gal staining
Postnatal cartilage development and growth are regulated by key growth factors and signaling molecules. To fully understand the function of these regulators, an inducible and chondrocyte-specific gene deletion system needs to be established to circumvent the perinatal lethality. In this report, we have generated a transgenic mouse model (Col2a1-CreERT2) in which expression of the Cre recombinase is driven by the chondrocyte-specific col2a1 promoter in a tamoxifen-inducible manner. To determine the specificity and efficiency of the Cre recombination, we have bred Col2a1-CreERT2 mice with Rosa26R reporter mice. The X-Gal staining showed that the Cre recombination is specifically achieved in cartilage tissues with tamoxifen-induction. In vitro experiments of chondrocyte cell culture also demonstrate the 4-hydroxy tamoxifen-induced Cre recombination. These results demonstrate that Col2a1-CreERT2 transgenic mice can be used as a valuable tool for an inducible and chondrocyte-specific gene deletion approach. genesis 45:44–50, 2007. Published 2007 Wiley-Liss, Inc.