About   Help   FAQ
Ses7129S6/SvEvTac
QTL Variant Detail
Summary
QTL variant: Ses7129S6/SvEvTac
Name: salmonella enteritidis susceptibility 7; 129S6/SvEvTac
MGI ID: MGI:3588702
QTL: Ses7  Location: Chr2:133306330-133306474 bp  Genetic Position: Chr2, cM position of peak correlated region/allele: 65.18 cM
QTL Note: genome coordinates based on the marker associated with the peak LOD score
Variant
origin
Strain of Specimen:  129S6/SvEvTac
Variant
description
Allele Type:    QTL
Inheritance:    Recessive
Phenotypes
Loading...
View phenotypes and curated references for all genotypes (concatenated display).
Notes

Mapping and Phenotype information for this QTL, its variants and associated markers

J:100367

Congenic lines were created to evaluate previously identified Salmonella susceptibility loci Ses1 (chr1), Ses2 (chr7), and Ses3 (chr15). Authors indicate that Ses1 is composed of 2 different linked loci, Ses1a (a.k.a. Ses1) and Ses1b (a.k.a. Ses1.1). Donor DNA from resistant strain C57BL/6J was introgressed onto the genetic background of susceptible strain 129S6/SvEvTac for each QTL. The effects of Ses1a (48.7 cM) and Ses1b (21 cM) on mouse Chromosome 1 were detected in the congenic lines. 129.B6-Ses1a and 129.B6-Ses1b lines cleared Salmonella infection significantly better than background strain 129S6/SvEvTac. The effects of Ses2 and Ses3 were not observed in the congenics.

A population of 300 (C57BL/6J x 129S6/SvEvTac)F2 animals were used to create a high density linkage map for linkage analysis. 244 microsatellite markers at an average spacing of 10.7 cM and 3 SNP markers were used for the genome scan. Ratio transmission distortion (RTD) was observed in a 40.7 cM interval on mouse Chromosome 7 between D7Mit228 and D7Mit237, which includes the Ses2 locus. The RTD region had a significantly high incidence of the homozygous C57BL/6J genotype (39%-41%) in female F2 mice compared to the expected incidence of 25%.

Ses1a was detected in a single-point linkage analysis. In female animals, Ses1a shows peak linkage at D1Mcg5 (39.3 cM; LOD=7.59) and in male animals Ses1a shows peak linkage at D1Mit19 (36.9 cM; LOD=4.4). C57BL/6J-derived alleles at Ses1a confer resistance to Salmonella infection with recessiveinheritance.

Two-point linkage analysis detected several novel interacting loci involved in the clearance of Salmonella infection. These new QTL, Ses4-Ses10, are discussed below.

In female F2 animals, Ses1a shows significant interaction with Ses4 at 14.2 cM near DXMit48 on mouse Chromosome X and Ses5 at 11 cM near D7Mit267 on mouse Chromosome 7. Female animals homozygous for C57BL/6J-derived alleles at both Ses1a and Ses4, or at both Ses1a and Ses5, show significant reduction in Salmonella bacterial load (~15-fold reduction) compared to female animals homozygous at Ses1a only. Ses4 and Ses5 do not exert an effect without Ses1a. A small effect on mouse Chromosome 15 attributed to Ses3 was also detected in female F2 animals.

In male F2 animals, significant interaction was detected between Ses1a and Ses6 at 4 cM near D9Mit218 on mouse Chromosome 9. Interacting locus pairs were also detected between Ses7 on mouse Chromosome 2 (D2Mit192; 76.3 cM) and Ses8 on mouse Chromosome 4 (D4Mit2; 6.5 cM), and between Ses9 on mouse Chromosome 3 (D3Mit256; 66.2 cM) and Ses10 on mouse Chromosome 13 (D13Mit36; 53 cM). C57BL/6J-derived alleles confer increased Salmonella clearance (reduced bacterial load) with recessive inheritance at all new male-specific loci, except at Ses7 which shows dominant inheritance. A significant effect on Salmonella clearance in male F2 animals was detected on mouse Chromosome 1 and is attributed to Ses1b.

References
Original:  J:100367 Caron J, et al., Mapping of interactions and mouse congenic strains identified novel epistatic QTLs controlling the persistence of Salmonella Enteritidis in mice. Genes Immun. 2005 Sep;6(6):500-8
All:  1 reference(s)

Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
Citing These Resources
Funding Information
Warranty Disclaimer, Privacy Notice, Licensing, & Copyright
Send questions and comments to User Support.
last database update
12/10/2024
MGI 6.24
The Jackson Laboratory