Segregation of a spontaneous Klrd1 (CD94) mutation in DBA/2 mouse substrains

Dai Lun Shin, Ashutosh K. Pandey, Jesse Dylan Ziebarth, Megan Mulligan, Robert Williams, Robert Geffers, Bastian Hatesuer, Klaus Schughart, Esther Wilk

Research output: Contribution to journalArticle

2 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)235-239
Number of pages5
JournalG3: Genes, Genomes, Genetics
Volume5
Issue number2
DOIs
StatePublished - Jan 1 2015

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Inbred DBA Mouse
Quantitative Trait Loci
Infectious Ectromelia
Mutation
Influenza A virus
Exons
Genes
Genetic Background

All Science Journal Classification (ASJC) codes

  • Molecular Biology
  • Genetics
  • Genetics(clinical)

Cite this

Segregation of a spontaneous Klrd1 (CD94) mutation in DBA/2 mouse substrains. / Shin, Dai Lun; Pandey, Ashutosh K.; Ziebarth, Jesse Dylan; Mulligan, Megan; Williams, Robert; Geffers, Robert; Hatesuer, Bastian; Schughart, Klaus; Wilk, Esther.

In: G3: Genes, Genomes, Genetics, Vol. 5, No. 2, 01.01.2015, p. 235-239.

Research output: Contribution to journalArticle

Shin, DL, Pandey, AK, Ziebarth, JD, Mulligan, M, Williams, R, Geffers, R, Hatesuer, B, Schughart, K & Wilk, E 2015, 'Segregation of a spontaneous Klrd1 (CD94) mutation in DBA/2 mouse substrains', G3: Genes, Genomes, Genetics, vol. 5, no. 2, pp. 235-239. https://doi.org/10.1534/g3.114.015164
Shin, Dai Lun ; Pandey, Ashutosh K. ; Ziebarth, Jesse Dylan ; Mulligan, Megan ; Williams, Robert ; Geffers, Robert ; Hatesuer, Bastian ; Schughart, Klaus ; Wilk, Esther. / Segregation of a spontaneous Klrd1 (CD94) mutation in DBA/2 mouse substrains. In: G3: Genes, Genomes, Genetics. 2015 ; Vol. 5, No. 2. pp. 235-239.
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