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

• Published in: Biochemical journal Vol. 443; no. 2; p. 355
• Main Authors: Kenneth, Niall S, Younger, J Michael, Hughes, Elizabeth D, Marcotte, Danielle, Barker, Philip A, Saunders, Thomas L, Duckett, Colin S
• Format: Journal Article
• Language: English
• Published: England 15.04.2012
• Subjects: Animals; Caspases - genetics; Caspases - metabolism; Cell Line; Enzyme Activation; Inhibitor of Apoptosis Proteins - deficiency; Inhibitor of Apoptosis Proteins - metabolism; Mice; Mice, 129 Strain; Mutation
• ISSN: 1470-8728
• DOI: 10.1042/bj20120249

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.