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Physiol. Genomics 35: 1-4, 2008. First published July 8, 2008; doi:10.1152/physiolgenomics.90284.2008
1094-8341/08 $8.00
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Received 3 July 2008; accepted in final form 7 July 2008.
Physiological Genomics 35:1-4 (2008)
1094-8341/08 $8.00 © 2008 American Physiological Society

Perspective

Germ line activation of the Tie2 and SMMHC promoters causes noncell-specific deletion of floxed alleles

Willem J. de Lange1, Carmen M. Halabi2, Andreas M. Beyer2 and Curt D. Sigmund1,3,4

1 Department of Internal Medicine, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa
2 Genetics Graduate Program, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa
3 Department of Molecular Physiology and Biophysics, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa
4 Center on Functional Genomics of Hypertension, Roy J. and Lucille A. Carver College of Medicine, University of Iowa, Iowa City, Iowa

Tissue-specific knockouts generated through Cre-loxP recombination have become an important tool to manipulate the mouse genome. Normally, two successive rounds of breeding are performed to generate mice carrying two floxed target-gene alleles and a transgene expressing Cre-recombinase tissue-specifically. We show herein that two promoters commonly used to generate endothelium-specific (Tie2) and smooth muscle-specific [smooth muscle myosin heavy chain (Smmhc)] knockout mice exhibit activity in the female and male germ lines, respectively. This can result in the inheritance of a null allele in the second generation that is not tissue specific. Careful experimental design is required therefore to ensure that tissue-specific knockouts are indeed tissue specific and that appropriate controls are used to compare strains.

Cre-loxP; knockout; conditional; vascular; endothelium; smooth muscle myosin heavy chain






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