Hbnr3^CBA
QTL Variant Detail

Summary

• QTL variant: Hbnr3^CBA
• Name: Heligmosomoides bakeri nematode resistance 3; CBA
• MGI ID: MGI:2660609
• QTL: Hbnr3 Location: Chr17:74107651-93507179 bp Genetic Position: Chr17, Syntenic

Variant origin

• Strain of Specimen: CBA

Variant description

• Allele Type: QTL
• Mutation: Undefined
• Mutation details: This allele confers resistance to infection by the nematode Heligmosomoides polygyrus compared to SWR.
• Inheritance: Recessive

Notes

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

J:82261

Linkage analysis was performed on an (SWR x CBA)F2 intercross population to identify loci affecting resistance/susceptibility to infection by the nematode Heligmosomoides polygyrus. Animals were orally infected with 125 larvae of H. polygyrus weekly for a period of 6 weeks. Parental strain SWR is resistant to nematode infection whereas CBA is susceptible. Loci with significant linkage were detected on mouse Chromosomes 1 and 17. Hpnr1 maps to 15 cM on mouse Chromosome 1 with LOD=12.52 for total worm count at D1Mit211. SWR-derived alleles appear to confer dominantly inherited resistance to nematode infection at Hpnr1. Hpnr2 and Hpnr3 map to 15.1 cM and 50.6 cM on mouse Chromosome 17, respectively. Hpnr2 is linked to total worm count with a LOD score of 4.28 at D17Mit29. SWR-derived alleles confer resistance to nematode infection at Hpnr2. Hpnr3 is linked to fecal egg count with a LOD score of 3.95 between D17Mit93 and D17Mit123. SWR-derived alleles confer dominantly inherited susceptibility to nematode infection at Hpnr3.

J:85787

500 (SWR x CBA)F2 animals were screened for 175 polymorphic markers to identify QTLs associated with immune response to gastrointestinal nematode infection. Parental strain SWR is resistant to infection by the nematode Heligmosomoides polygyrus compared to susceptible parental strain CBA. Following infection with Heligmosomoides polygyrus, parental strain CBA exhibits increase ganuloma scores (GS), increased IgG1, decreased IgE, and decreased levels of mucosal mast cell protease 1 (MMCP1).

Previously identified QTLs Hpnr1, Hpnr2, and Hpnr3 were detected in this study. Hpnr1 reached LOD=8.4 at 21 cM on mouse Chromosome 1 between D1Mit211 (15 cM) and D1Mit214 (43 cM). SWR-derived alleles confer decreased fecal egg count and total worm count with dominantinheritance at Hpnr1. Hprn2 reached LOD=5.02 at 17 cM on mouse Chromosome 17 between D17Mit29 (15.1 cM) and D17Mit176 (24 cM). SWR-derived alleles confer increased granuloma scores with dominant inheritance at Hnpr2. Hprn3 reached LOD=2.56 at 57 cM on mouse Chromosome 17 between D17Mit93 (50 cM) and D17Mit123 (57 cM). SWR-derived alleles confer increased fecal egg count and total worm count with dominant inheritance at Hnpr3.

The following novel QTL reaching a statistical significant of P>0.01 were identified:

Hpnr4 mapped to 85 cM on mouse Chromosome 1 with LOD=3.07 between D1Mit102 (73 cM) and D1Mit362 (106.3 cM). SWR-derived alleles confer increased MMCP1 levels with recessive inheritance at Hpnr4.

Hpnr5 mapped to 30 cM on mouse Chromosome 2 withLOD=2.79 between D2Mit296 (18 cM) and D2Mit44 (47 cM). SWR-derived alleles confer decreased fecal egg count and total worm count with dominant inheritance at Hpnr5.

Hpnr6 mapped to 44 cM on mouse Chromosome 12 with LOD=4.13 between D12Mit177 (36 cM) andD12Mit194 (45 cM). SWR-derived alleles confer increased in IgE levels with recessive inheritance at Hpnr6.

Hpnr7 mapped to 32 cM on mouse Chromosome 17 with LOD=6.15 between D17Mit176 (22 cM) and D17Mit180 (40.2 cM). SWR-derived alleles confer decreasedIgG1 levels with dominant inheritance at Hpnr7.

Hpnr8 mapped to 36 cM on mouse Chromosome 19 with LOD=2.77 between D19Mit88 (34 cM) and D19Mit89 (41 cM). SWR-derived alleles confer decreased fecal egg count and total worm count with dominant inheritanceat Hprn8.

References

• Original: J:82261 Iraqi FA, et al., Chromosomal regions controlling resistance to gastro-intestinal nematode infections in mice. Mamm Genome. 2003 Mar;14(3):184-91
• All: 2 reference(s)