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Nucleic Acids Research, 2003, Vol. 31, No. 10 e57
© 2003 Oxford University Press

An inbred 129SvEv GFPCre transgenic mouse that deletes loxP-flanked genes in all tissues

John R. Scheel, Lisa J. Garrett1, Duane M. Allen, Todd A. Carter, Lynne Randolph-Moore, Micheal J. Gambello2, Fred H. Gage, Anthony Wynshaw-Boris2 and Carrolee Barlow

The Salk Institute for Biological Studies, Laboratory of Genetics, 10010 North Torrey Pines Road, San Diego, CA 92037, USA, 1 National Institutes of Health, Genetics and Molecular Biology Laboratory, Building 49, Room 4A69, 49 Convent Drive, Bethesda, MD 20892, USA and 2 Biomedical Sciences Program, University of California, San Diego, La Jolla, CA 92093-0627, USA

The authors wish it to be known that, in their opinion, the first two authors should be regarded as joint First Authors

A common method for generating mice with subtle genetic manipulations uses homologous recombination (HR) in embryonic stem (ES) cells to replace a wild-type gene with a slightly modified one. Generally, a drug resistance gene is inserted with the modified gene to select correctly targeted clones. Often, however, the presence of this drug resistance gene interferes with the normal locus and creates a null or hypomorphic allele. Flanking of the selectable marker by loxP sites followed by Cre-mediated deletion after drug selection can overcome this problem. The simplest method used to remove a loxP-flanked selectable marker is to breed an animal carrying a loxP-flanked drug resistance gene to an animal that expresses Cre recombinase in the germline. To date only outbred transgenic mice are available for this purpose. This can be problematic for phenotypic analysis in many organ systems, including the brain, and for the analysis of behavior. While attempting to make 129S6/SvEvTac inbred background (isogenic to our ES cells) mice that express Cre under the control of several tissue-specific promoters, we serendipitously generated a line that excises loxP-flanked drug resistance genes in all tissues, including the germline. This reagent allows deletion of loxP-flanked sequences while maintaining the mutation on an inbred background.


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