2.50
Hdl Handle:
http://hdl.handle.net/10033/614883
Title:
Segregation of a spontaneous Klrd1 (CD94) mutation in DBA/2 mouse substrains.
Authors:
Shin, Dai-Lun; Pandey, Ashutosh K; Ziebarth, Jesse Dylan; Mulligan, Megan K; Williams, Robert W; Geffers, Robert ( 0000-0003-4409-016X ) ; Hatesuer, Bastian; Schughart, Klaus ( 0000-0002-6824-7523 ) ; Wilk, Esther ( 0000-0003-3446-5511 )
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.
Affiliation:
Helmholtz Centre for infection research, Inhoffenstr. 7, 38124 Braunschweig, Germany.
Citation:
Segregation of a spontaneous Klrd1 (CD94) mutation in DBA/2 mouse substrains. 2015, 5 (2):235-9 G3 (Bethesda)
Journal:
G3 (Bethesda, Md.)
Issue Date:
Feb-2015
URI:
http://hdl.handle.net/10033/614883
DOI:
10.1534/g3.114.015164
PubMed ID:
25520036
Type:
Article
Language:
en
ISSN:
2160-1836
Appears in Collections:
publications of the department infection genetics (INFG)

Full metadata record

DC FieldValue Language
dc.contributor.authorShin, Dai-Lunen
dc.contributor.authorPandey, Ashutosh Ken
dc.contributor.authorZiebarth, Jesse Dylanen
dc.contributor.authorMulligan, Megan Ken
dc.contributor.authorWilliams, Robert Wen
dc.contributor.authorGeffers, Roberten
dc.contributor.authorHatesuer, Bastianen
dc.contributor.authorSchughart, Klausen
dc.contributor.authorWilk, Estheren
dc.date.accessioned2016-06-28T08:58:32Z-
dc.date.available2016-06-28T08:58:32Z-
dc.date.issued2015-02-
dc.identifier.citationSegregation of a spontaneous Klrd1 (CD94) mutation in DBA/2 mouse substrains. 2015, 5 (2):235-9 G3 (Bethesda)en
dc.identifier.issn2160-1836-
dc.identifier.pmid25520036-
dc.identifier.doi10.1534/g3.114.015164-
dc.identifier.urihttp://hdl.handle.net/10033/614883-
dc.description.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.en
dc.language.isoenen
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/4.0/*
dc.subject.meshAnimalsen
dc.subject.meshFemaleen
dc.subject.meshMice, Inbred DBAen
dc.subject.meshMutationen
dc.subject.meshNK Cell Lectin-Like Receptor Subfamily Den
dc.subject.meshQuantitative Trait Locien
dc.titleSegregation of a spontaneous Klrd1 (CD94) mutation in DBA/2 mouse substrains.en
dc.typeArticleen
dc.contributor.departmentHelmholtz Centre for infection research, Inhoffenstr. 7, 38124 Braunschweig, Germany.en
dc.identifier.journalG3 (Bethesda, Md.)en
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