title: Segregation of a spontaneous Klrd1 (CD94) mutation in DBA/2 mouse substrains.
abstract: Current model DBA/2J (D2J) mice lack CD94 expression due to a deletion spanning the last coding exon of the Klrd1 gene that occurred in the mid- to late 1980s. In contrast, DBA/2JRj (D2Rj) mice, crosses derived from DBA/2J before 1984, and C57BL/6J (B6) mice lack the deletion and have normal CD94 expression. For example, BXD lines (BXD1-32) generated in the 1970s by crossing B6 and D2J do not segregate for the exonic deletion and have high expression, whereas BXD lines 33 and greater were generated after 1990 are segregating for the deletion and have highly variable Klrd1 expression. We performed quantitative trait locus analysis of Klrd1 expression by using BXD lines with different generation times and found that the expression difference in Klrd1 in the later BXD set is driven by a strong cis-acting expression quantitative trait locus. Although the Klrd1/CD94 locus is essential for mousepox resistance, the genetic variation among D2 substrains and the later set of BXD strains is not associated with susceptibility to the Influenza A virus PR8 strain. Substrains with nearly identical genetic backgrounds that are segregating functional variants such as the Klrd1 deletion are useful genetic tools to investigate biological function.
authors.affiliation: Department of Infection Genetics, Helmholtz Centre for Infection Research and University of Veterinary Medicine Hannover, Braunschweig, Germany.
authors.forename: Dai-Lun
authors.initials: DL
authors.lastname: Shin
authors.affiliation: Department of Genetics, Genomics and Informatics, Center for Integrative and Translational Genomics, University of Tennessee Health Science Center, Memphis, Tennessee.
authors.forename: Ashutosh K
authors.initials: AK
authors.lastname: Pandey
authors.affiliation: Department of Genetics, Genomics and Informatics, Center for Integrative and Translational Genomics, University of Tennessee Health Science Center, Memphis, Tennessee.
authors.forename: Jesse Dylan
authors.initials: JD
authors.lastname: Ziebarth
authors.affiliation: Department of Genetics, Genomics and Informatics, Center for Integrative and Translational Genomics, University of Tennessee Health Science Center, Memphis, Tennessee.
authors.forename: Megan K
authors.initials: MK
authors.lastname: Mulligan
authors.affiliation: Department of Genetics, Genomics and Informatics, Center for Integrative and Translational Genomics, University of Tennessee Health Science Center, Memphis, Tennessee.
authors.forename: Robert W
authors.initials: RW
authors.lastname: Williams
authors.affiliation: Research Group Genome Analytics, Helmholtz Centre for Infection Research, Braunschweig, Germany.
authors.forename: Robert
authors.initials: R
authors.lastname: Geffers
authors.affiliation: Department of Infection Genetics, Helmholtz Centre for Infection Research and University of Veterinary Medicine Hannover, Braunschweig, Germany.
authors.forename: Bastian
authors.initials: B
authors.lastname: Hatesuer
authors.affiliation: Department of Genetics, Genomics and Informatics, Center for Integrative and Translational Genomics, University of Tennessee Health Science Center, Memphis, Tennessee.
authors.forename: Klaus
authors.initials: K
authors.lastname: Schughart
authors.affiliation: Department of Infection Genetics, Helmholtz Centre for Infection Research and University of Veterinary Medicine Hannover, Braunschweig, Germany Esther.Wilk@helmholtz-hzi.de.
authors.forename: Esther
authors.initials: E
authors.lastname: Wilk
mesh_terms: D000818:Animals; D005260:Female; D008811:Mice, Inbred DBA / Q000235:genetics*; D009154:Mutation; D051920:NK Cell Lectin-Like Receptor Subfamily D / Q000235:genetics*; D040641:Quantitative Trait Loci
chemical_list: D051920:NK Cell Lectin-Like Receptor Subfamily D
keywords: BXD; DBA/2; Klrd1