early conceptus |
embryo ectoderm |
embryo endoderm |
embryo mesoderm |
embryo mesenchyme |
extraembryonic component |
alimentary system |
auditory system |
branchial arches |
cardiovascular system |
connective tissue |
endocrine system |
exocrine system |
hemolymphoid system |
integumental system |
limbs |
liver and biliary system |
musculoskeletal system |
nervous system |
olfactory system |
reproductive system |
respiratory system |
urinary system |
visual system |
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Transcription Start Site | Location | Distance from Gene 5'-end |
| Tssr26335 | Chr2:130905428-130905479 (-) | 280 bp |
| Tssr26334 | Chr2:130898501-130898530 (-) | 7,218 bp |
| Tssr26333 | Chr2:130898485-130898496 (-) | 7,243 bp |
| Tssr26332 | Chr2:130897746-130897750 (-) | 7,986 bp |
| Tssr26331 | Chr2:130896432-130896473 (-) | 9,281 bp |
| QTL | Genetic Location* | Genome Location (GRCm39) | Reference | QTL Note |
| Bhr1 | Chr2, syntenic | Chr2:142593476-178442452 | J:97472 | Linkage analysis was performed on 123 recombinant congenic animals at the N8 generation to identify QTLs associated with airway hyperresponsiveness (AHR). A recombinant congenic line was created by repeated backcrossing of (C57BL/6J x A/J)F1 animals to C57BL/6J for 7 generations and selecting for the AHR phenotype at each generation. Donor strain A/J exhibits increased naive AHR compared to background strain C57BL/6J. At generation N8 the recombinant congenic line displayed 80% of the donor A/J AHR phenotype. This line retained A/J-derived donor DNA on chromosomes 2 from D2Mit259 - D2Mit148, chromosome 6 from D6Mit86 - D6Mit9, and chromosome 10 from D10Mit95 - D10Mit103. When analyzed separately the loci on chromosomes 2 (Bhr1) and 6 (Bhr8) show only asuggestive linkage to AHR. The combined effect of these 2 loci when inherited together show a highly significant linkage to AHR with LOD=5.5, and explains 18.7% of the total variance. It is believed that A/J-derived alleles confer dominantly inherited susceptibility to AHR. The region of the human genome that has conserved syntenty with the retained A/J regions of chromosome 2 and 6 is large. Human studies have associated SNPs in the ADAM33 gene with asthma. It is notable that metalloprotease Adam33 is located in the retained region on chromosome 2. Recent data in the mouse suggest that differences in Adam33 activity are not likely to account for the strain-specific AHR phenotypes, as a multistrain comparison of 198 potential SNPs in Adam33 genomic sequences (including extensive upstream and downstream regions) found that none differed bewteen the A/J and C57BL/6J strains. (http://mousesnp.roche.com/). Also, dipeptidyl peptidase, DPP10 was found to be associated with asthma in humans and was also reported to be in a region of conserved synteny with mouse loci on chromosome 2 linked to elevated AHR. However, the mouse ortholog of DPP10 (GenBank: AK046842) maps to mouse chromosome 1 and is consequently not a candiate for causing elevated AHR in A/J mice. |
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO) |
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last database update 03/18/2025 MGI 6.24 |
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