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Cell Rep. 2016 May 31;15(9):1901-9. doi: 10.1016/j.celrep.2016.04.080. Epub 2016 May 19.

Striking Immune Phenotypes in Gene-Targeted Mice Are Driven by a Copy-Number Variant Originating from a Commercially Available C57BL/6 Strain.

Author information

1
Ragon Institute of MGH, MIT and Harvard, 400 Technology Square, Cambridge, MA 02139, USA.
2
Departments of Medicine and Cellular and Molecular Medicine, University of California, San Diego, La Jolla, CA 92093, USA.
3
Ragon Institute of MGH, MIT and Harvard, 400 Technology Square, Cambridge, MA 02139, USA. Electronic address: pillai@helix.mgh.harvard.edu.

Abstract

We describe a homozygous copy-number variant that disrupts the function of Dock2 in a commercially available C57BL/6 mouse strain that is widely used for backcrossing. This Dock2 allele was presumed to have spontaneously arisen in a colony of Irf5 knockout mice. We discovered that this allele has actually been inadvertently backcrossed into multiple mutant mouse lines, including two engineered to be deficient in Siae and Cmah. This particular commercially obtained subline of C57BL/6 mice also exhibits several striking immune phenotypes that have been previously described in the context of Dock2 deficiency. Inadvertent backcrossing of a number of gene-targeted mice into this background has complicated the interpretation of several immunological studies. In light of these findings, published studies involving immune or hematopoietic phenotypes in which these C57BL/6 mice have been used as controls, as experimental animals, or for backcrossing will need to be reinterpreted.

PMID:
27210752
PMCID:
PMC4892502
DOI:
10.1016/j.celrep.2016.04.080
[Indexed for MEDLINE]
Free PMC Article

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