Segregation of a spontaneous Klrd1 (CD94) mutation in DBA/2 mouse substrains.
Cast your vote
You can rate an item by clicking the amount of stars they wish to award to this item.
When enough users have cast their vote on this item, the average rating will also be shown.
Your vote was cast
Thank you for your feedback
Thank you for your feedback
Pandey, Ashutosh K
Ziebarth, Jesse Dylan
Mulligan, Megan K
Williams, Robert W
MetadataShow full item record
AbstractCurrent 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.
CitationSegregation of a spontaneous Klrd1 (CD94) mutation in DBA/2 mouse substrains. 2015, 5 (2):235-9 G3 (Bethesda)
AffiliationHelmholtz Centre for infection research, Inhoffenstr. 7, 38124 Braunschweig, Germany.
JournalG3 (Bethesda, Md.)
The following license files are associated with this item:
Except where otherwise noted, this item's license is described as http://creativecommons.org/licenses/by-nc-sa/4.0/
- Dependency of intraocular pressure elevation and glaucomatous changes in DBA/2J and DBA/2J-Rj mice.
- Authors: Scholz M, Buder T, Seeber S, Adamek E, Becker CM, Lütjen-Drecoll E
- Issue date: 2008 Feb
- Determining immune components necessary for progression of pigment dispersing disease to glaucoma in DBA/2J mice.
- Authors: Nair KS, Barbay J, Smith RS, Masli S, John SW
- Issue date: 2014 Mar 28
- The Hcr (hepatocarcinogen resistance) loci of DBA/2J mice partially suppress phenotypic expression of the Hcs (hepatocarcinogen sensitivity) loci of C3H/HeJ mice.
- Authors: Lee GH, Drinkwater NR
- Issue date: 1995 Aug
- Genetic architecture of fast- and slow-twitch skeletal muscle weight in 200-day-old mice of the C57BL/6J and DBA/2J lineage.
- Authors: Lionikas A, Blizard DA, Vandenbergh DJ, Glover MG, Stout JT, Vogler GP, McClearn GE, Larsson L
- Issue date: 2003 Dec 16
- Segregation analysis of the testis-determining autosomal trait, Tda, that differs between the C57Bl/6J and DBA/2J mouse strains suggests a multigenic threshold model.
- Authors: Eisner JR, Eales BA, Biddle FG
- Issue date: 1996 Apr