An inactivating caspase 11 passenger mutation originating from the 129 murine strain in mice targeted for c-IAP1

Author:

Kenneth Niall S.1,Younger J. Michael1,Hughes Elizabeth D.2,Marcotte Danielle3,Barker Philip A.3,Saunders Thomas L.24,Duckett Colin S.145

Affiliation:

1. Department of Pathology, University of Michigan, Ann Arbor, MI 48109, U.S.A.

2. Transgenic Animal Model Core, University of Michigan, Ann Arbor, MI 48109, U.S.A.

3. Department of Neurology and Neurosurgery, Montreal Neurological Institute, McGill University, 3801 University Street, Montreal, QC, Canada, H3A 2B4

4. Department of Internal Medicine, University of Michigan, Ann Arbor, MI 48109, U.S.A.

5. Comprehensive Cancer Center, University of Michigan, Ann Arbor, MI 48109, U.S.A.

Abstract

A recent study revealed that ES (embryonic stem) cell lines derived from the 129 murine strain carry an inactivating mutation within the caspase 11 gene (Casp4) locus [Kayagaki, Warming, Lamkanfi, Vande Walle, Louie, Dong, Newton, Qu, Liu, Heldens, Zhang, Lee, Roose-Girma and Dixit (2011) Nature 479, 117–121]. Thus, if 129 ES cells are used to target genes closely linked to caspase 11, the resulting mice might also carry the caspase 11 deficiency as a passenger mutation. In the present study, we examined the genetic loci of mice targeted for the closely linked c-IAP (cellular inhibitor of apoptosis) genes, which were generated in 129 ES cells, and found that, despite extensive backcrossing into a C57BL/6 background, c-IAP1−/− animals are also deficient in caspase 11. Consequently, data obtained from these mice should be re-evaluated in this new context.

Publisher

Portland Press Ltd.

Subject

Cell Biology,Molecular Biology,Biochemistry

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