Striking Immune Phenotypes in Gene-Targeted Mice Are Driven by a Copy-Number Variant Originating from a Commercially Available C57BL/6 Strain
Name
Mahajan-2016-Striking Immune Phen.pdf
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3.15 MB
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Author(s)
Mahajan, Vinay S.
Demissie, Ezana
Mattoo, Hamid
Viswanadham, Vinay
Varki, Ajit
Morris, Robert
Pillai, Shiv
Mahajan, Vinay S.
Date Issued
May 2016
Journal
Cell Reports
Publisher
Elsevier
Citation
Mahajan, Vinay S., Ezana Demissie, Hamid Mattoo, Vinay Viswanadham, Ajit Varki, Robert Morris, and Shiv Pillai. “Striking Immune Phenotypes in Gene-Targeted Mice Are Driven by a Copy-Number Variant Originating from a Commercially Available C57BL/6 Strain.” Cell Reports 15:9 (May 2016), pp.1901-1909.
Version
Final published version
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.
MIT Department
Massachusetts Institute of Technology. Department of Biological Engineering
Ragon Institute of MGH, MIT and Harvard
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Creative Commons Attribution-NonCommercial-NoDerivs License
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DOI of Published Version
https://doi.org/10.1016/j.celrep.2016.04.080
