Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow Print PDF (466K) Freely available
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Dragatsis, I.
Right arrow Articles by Zeitlin, S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Dragatsis, I.
Right arrow Articles by Zeitlin, S.
Related Collections
Right arrow Mutagenesis
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 2001, Vol. 29, No. 3 e10
© 2001 Oxford University Press

A method for the generation of conditional gene repair mutations in mice

Ioannis Dragatsis and Scott Zeitlin1,*

Department of Genetics and Development and 1Department of Pathology, Columbia University, New York, NY 10032, USA

Conditional gene repair mutations in the mouse can assist in cell lineage analyses and provide a valuable complement to conditional gene inactivation strategies. We present a method for the generation of conditional gene repair mutations that employs a loxP-flanked (floxed) selectable marker and transcriptional/translational stop cassette (neostop) located within the first intron of a target gene. In the absence of Cre recombinase, expression of the targeted allele is suppressed generating a null allele, while in the presence of Cre, excision of neostop restores expression to wild-type levels. To test this strategy, we have generated a conditional gene repair allele of the mouse Huntington’s disease gene homolog (Hdh). Insertion of neostop within the Hdh intron 1 generated a null allele and mice homozygous for this allele resembled nullizygous Hdh mutants and died after embryonic day 8.5. In the presence of a cre transgene expressed ubiquitously early in development, excision of neostop restored Hdh expression and rescued the early embryonic lethality. A simple modification of this strategy that permits the generation of conventional gene knockout, conditional gene knockout and conditional gene repair alleles using one targeting construct is discussed.

* To whom correspondence should be addressed at present address: Department of Neuroscience, University of Virginia School of Medicine, PO Box 801392, Charlottesville, VA 22908-1392, USA. Tel: +1 804 924 5011; Fax: +1 804 982 4380; Email: soz4n{at}virginia.edu


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Hum Mol GenetHome page
I. Dragatsis, S. Zeitlin, and P. Dietrich
Huntingtin-associated protein 1 (Hap1) mutant mice bypassing the early postnatal lethality are neuroanatomically normal and fertile but display growth retardation
Hum. Mol. Genet., December 15, 2004; 13(24): 3115 - 3125.
[Abstract] [Full Text] [PDF]

Home page
 Nucleic Acids ResHome page
K. Araki, M. Araki, and K.-i. Yamamura
Site-directed integration of the cre gene mediated by Cre recombinase using a combination of mutant lox sites
Nucleic Acids Res., October 1, 2002; 30(19): e103 - e103.
[Abstract] [Full Text] [PDF]


Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.