Ses9^C57BL/6J
QTL Variant Detail

Summary

• QTL variant: Ses9^C57BL/6J
• Name: salmonella enteritidis susceptibility 9; C57BL/6J
• MGI ID: MGI:3588707
• QTL: Ses9 Location: Chr3:136057332-136057456 bp Genetic Position: Chr3, cM position of peak correlated region/allele: 63.04 cM
• QTL Note: genome coordinates based on the marker associated with the peak LOD score

Variant origin

• Strain of Specimen: C57BL/6J

Variant description

• Allele Type: QTL
• Mutation: Undefined
• Mutation details: This allele confers resistance to Salmonella enteritidis infection in male animals compared to 129S6/SvEvTac. (J:100367)
• Inheritance: Recessive

Notes

Ses9 does not have an effect without Ses10. Male animals homzoygous for C57BL/6J-derived alleles at both Ses9 and Ses10 exhibit significantly reduced Salmonella bacterial loads.

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)