TY - JOUR
T1 - Cutting edge
T2 - Check your mice - A point mutation in the Ncr1 locus identified in CD45.1 congenic mice with consequences in mouse susceptibility to infection
AU - Jang, Youngsoon
AU - Gerbec, Zachary J.
AU - Won, Taejoon
AU - Choi, Bongkum
AU - Podsiad, Amy
AU - Moore, Bethany B.
AU - Malarkannan, Subramaniam
AU - Laouar, Yasmina
N1 - Funding Information:
This work was supported by National Institutes of Health Grants R01 AI102893 and R01 CA179363 (to S.M.), R01 HL119682 (to B.B.M.), and R01 AI083642 (to Y.L.), the Midwest Athletes Against Childhood Cancer Fund (to S.M.), the Gardetto Family
Publisher Copyright:
© 2018 by The American Association of Immunologists, Inc.
PY - 2018/3/15
Y1 - 2018/3/15
N2 - B6.SJL-Ptprca Pepcb/Boy (CD45.1) mice have been used in hundreds of congenic competitive transplants, with the presumption that they differ from C57BL/6 mice only at the CD45 locus. In this study, we describe a point mutation in the natural cytotoxicity receptor 1 (Ncr1) locus fortuitously identified in the CD45.1 strain. This point mutation was mapped at the 40th nucleotide of the Ncr1 locus causing a single amino acid mutation from cysteine to arginine at position 14 from the start codon, resulting in loss of NCR1 expression. We found that these mice were more resistant to CMV due to a hyper innate IFN-γ response in the absence of NCR1. In contrast, loss of NCR1 increased susceptibility to influenza virus, a result that is consistent with the role of NCR1 in the recognition of influenza Ag, hemagglutinin. This work sheds light on potential confounding experimental interpretation when this congenic strain is used as a tool for tracking lymphocyte development.
AB - B6.SJL-Ptprca Pepcb/Boy (CD45.1) mice have been used in hundreds of congenic competitive transplants, with the presumption that they differ from C57BL/6 mice only at the CD45 locus. In this study, we describe a point mutation in the natural cytotoxicity receptor 1 (Ncr1) locus fortuitously identified in the CD45.1 strain. This point mutation was mapped at the 40th nucleotide of the Ncr1 locus causing a single amino acid mutation from cysteine to arginine at position 14 from the start codon, resulting in loss of NCR1 expression. We found that these mice were more resistant to CMV due to a hyper innate IFN-γ response in the absence of NCR1. In contrast, loss of NCR1 increased susceptibility to influenza virus, a result that is consistent with the role of NCR1 in the recognition of influenza Ag, hemagglutinin. This work sheds light on potential confounding experimental interpretation when this congenic strain is used as a tool for tracking lymphocyte development.
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U2 - 10.4049/jimmunol.1701676
DO - 10.4049/jimmunol.1701676
M3 - Article
C2 - 29440507
AN - SCOPUS:85044713946
SN - 0022-1767
VL - 200
SP - 1982
EP - 1987
JO - Journal of Immunology
JF - Journal of Immunology
IS - 6
ER -