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Segregation of a Spontaneous Klrd1 (CD94) Mutation in DBA/2 Mouse Substrains

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 ex...

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Autores principales: Shin, Dai-Lun, Pandey, Ashutosh K., Ziebarth, Jesse Dylan, Mulligan, Megan K., Williams, Robert W., Geffers, Robert, Hatesuer, Bastian, Schughart, Klaus, Wilk, Esther
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Genetics Society of America 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4321031/
https://www.ncbi.nlm.nih.gov/pubmed/25520036
http://dx.doi.org/10.1534/g3.114.015164
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author Shin, Dai-Lun
Pandey, Ashutosh K.
Ziebarth, Jesse Dylan
Mulligan, Megan K.
Williams, Robert W.
Geffers, Robert
Hatesuer, Bastian
Schughart, Klaus
Wilk, Esther
author_facet Shin, Dai-Lun
Pandey, Ashutosh K.
Ziebarth, Jesse Dylan
Mulligan, Megan K.
Williams, Robert W.
Geffers, Robert
Hatesuer, Bastian
Schughart, Klaus
Wilk, Esther
author_sort Shin, Dai-Lun
collection PubMed
description 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.
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spelling pubmed-43210312015-02-18 Segregation of a Spontaneous Klrd1 (CD94) Mutation in DBA/2 Mouse Substrains Shin, Dai-Lun Pandey, Ashutosh K. Ziebarth, Jesse Dylan Mulligan, Megan K. Williams, Robert W. Geffers, Robert Hatesuer, Bastian Schughart, Klaus Wilk, Esther G3 (Bethesda) Investigations 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. Genetics Society of America 2014-12-17 /pmc/articles/PMC4321031/ /pubmed/25520036 http://dx.doi.org/10.1534/g3.114.015164 Text en Copyright © 2015 Shin et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution Unported License (http://creativecommons.org/licenses/by/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Investigations
Shin, Dai-Lun
Pandey, Ashutosh K.
Ziebarth, Jesse Dylan
Mulligan, Megan K.
Williams, Robert W.
Geffers, Robert
Hatesuer, Bastian
Schughart, Klaus
Wilk, Esther
Segregation of a Spontaneous Klrd1 (CD94) Mutation in DBA/2 Mouse Substrains
title Segregation of a Spontaneous Klrd1 (CD94) Mutation in DBA/2 Mouse Substrains
title_full Segregation of a Spontaneous Klrd1 (CD94) Mutation in DBA/2 Mouse Substrains
title_fullStr Segregation of a Spontaneous Klrd1 (CD94) Mutation in DBA/2 Mouse Substrains
title_full_unstemmed Segregation of a Spontaneous Klrd1 (CD94) Mutation in DBA/2 Mouse Substrains
title_short Segregation of a Spontaneous Klrd1 (CD94) Mutation in DBA/2 Mouse Substrains
title_sort segregation of a spontaneous klrd1 (cd94) mutation in dba/2 mouse substrains
topic Investigations
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4321031/
https://www.ncbi.nlm.nih.gov/pubmed/25520036
http://dx.doi.org/10.1534/g3.114.015164
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