Journal
IMMUNITY
Volume 43, Issue 1, Pages 200-209Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2015.06.011
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Funding
- Foundation against Cancer [2012-188]
- Flemish Government [BOF09/01M00709]
- European grant (FP6 ApopTrain) [MRTNCT-035624]
- European grant (FP7 EC RTD Integrated Project, Apo-Sys) [FP7-200767]
- European grant (Euregional PACT II)
- Belgian grants (Interuniversity Attraction Poles) [IAP 6/18, IAP 7/32]
- Flemish grants (Research Foundation Flanders) [FWO G.0875.11, FWO G.0973.11 N, FWO G.0A45.12 N, FWO G.0172.12, FWO G.0787.13N, G0C3114N, FWO KAN 31528711]
- Flemish grants (Foundation against Cancer) [2012-188]
- Ghent University grants (MRP, GROUP-ID consortium)
- Flanders Institute for Biotechnology (VIB)
- Methusalem grant
- NIH R01 grant from USA [EY021517]
- FWO
- Ghent University grants
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Targeted mutagenesis in mice is a powerful tool for functional analysis of genes. However, genetic variation between embryonic stem cells (ESCs) used for targeting (previously almost exclusively 129-derived) and recipient strains (often C57BL/6J) typically results in congenic mice in which the targeted gene is flanked by ESC-derived passenger DNA potentially containing mutations. Comparative genomic analysis of 129 and C57BL/6J mouse strains revealed indels and single nucleotide polymorphisms resulting in alternative or aberrant amino acid sequences in 1,084 genes in the 129-strain genome. Annotating these passenger mutations to the reported genetically modified congenic mice that were generated using 129-strain ESCs revealed that nearly all these mice possess multiple passenger mutations potentially influencing the phenotypic outcome. We illustrated this phenotypic interference of 129-derived passenger mutations with several case studies and developed a Me-PaMuFind-It web tool to estimate the number and possible effect of passenger mutations in transgenic mice of interest.
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