Abhr2 QTL Detail

Summary

• Symbol
  Abhr2
• Name
  antigen-induced bronchial hyperresponsiveness 2

• Feature Type
  QTL
• IDs
  MGI:1888529
  NCBI Gene: 109521
• Candidate Genes
  3 Genes

Location &
Maps

• Sequence Map
  Genome coordinates not available from the current reference assembly.

• Genetic Map
  Chromosome 2, 22.83 cM (cM position of peak correlated region/marker)
• Mapping Data
  3 experiments

Mutations,
Alleles, and
Phenotypes

• Phenotype Summary
  2 phenotype references
  

• All Mutations and Alleles
  2
• QTL
  2
• Find Mice (IMSR)
  0 strains or lines available

Sequences &
Gene Models

• NCBI Gene
  109521

References

• Summaries
  All 4

  Phenotypes 2
• Earliest
  J:66641 Ewart SL, et al., Quantitative trait loci controlling allergen-induced airway hyperresponsiveness in inbred mice. Am J Respir Cell Mol Biol. 2000 Oct;23(4):537-45
• Latest
  J:122917 Li X, et al., Fine mapping of murine asthma quantitative trait loci and analyses of Ptgs1 and Mrc1 as positional candidate genes. DNA Seq. 2007 Jun;18(3):190-5

Candidate Genes for Abhr2:

Gene	Genome Location (GRCm39)	Reference	QTL Note
Hc	Chr2:34873343-34951450 (-)	J:108211	Abhr2 (allergen induced bronchial hyperresponsiveness 2) is a previously identified QTL at approximately 30 cM on mouse Chromosome 2. Gene expression microarray analysis of lung RNA extracted from sensitive high-responder strain A/J and resistant low-responder strain C3H/HeJ, as well as low- and high-responding (A/J x C3H/HeJ)F1 x A/J backcross animals. Twenty-one differentially expressed genes were identified one of which, Hc (formerly C5), mapped near Abhr2 at 23.5 cM on chromosome 2. Hc mRNA expression patterns correlated with bronchial hyperresponsive phenotype- A/J and high-responder backcross animals exhibit high Hc expression whereas C3H/HeJ and low-responder backcross animals exhibit low Hc expression. In addition, Hc genotype also correlated with severity of bronchial hyperresponsiveness in backcross animals. Homozygosity for A/J-derived alleles at Hc was associated with high responsiveness while heterozygosity at Hc was associated with low responsiveness. Hc SNP analysis revealed a 2 bp deletion in the sensitive A/J strain resulting in deficient Hc mRNA and protein production. Resistant strain C3H/HeJ does not have this mutation and produces functional Hc mRNA and protein. This SNP was screened in other inbred strains with known bronchial hyperresponsive phenotypes. The 2 bp Hc deletion was observed in sensitive strains AKR/J and A/J, but not in resistant strains C57BL/6J, BALB/cJ, and C3H/HeJ.
Mrc1	Chr2:14234225-14336834 (+)	J:122917	The present study fine maps two previously identified airway hyper-responsiveness QTLs on mouse Chromosome 2 named Abhr1 (10 cM) and Abhr2 (30 cM). Thirty-seven polymorphic chromosome 2 markers were genotyped in 450 (C3H/HeJ x A/J)F1 x A/J backcross animals. Mrc1 at 5 cM was identified as a potential candidate gene for Abhr1. Ptgs1 at 29 cM was identified as a potential candidate gene for Abhr2. Sequence analysis of Mrc1 and Ptgs1 sequences did not detect polymorphism between A/J and C3H/HeJ. Gene expression analysis of Mrc1 and Ptgs1 lung mRNA following induction of allergic asthma in A/J and C3H/HeJ animals was performed. Ptgs1 was found to be downregulated in both inbred strains 72 hours after allergic asthma induction; however a strain-specific expression difference was not detected.
Ptgs1	Chr2:36120438-36142284 (+)	J:122917	The present study fine maps two previously identified airway hyper-responsiveness QTLs on mouse Chromosome 2 named Abhr1 (10 cM) and Abhr2 (30 cM). Thirty-seven polymorphic chromosome 2 markers were genotyped in 450 (C3H/HeJ x A/J)F1 x A/J backcross animals. Mrc1 at 5 cM was identified as a potential candidate gene for Abhr1. Ptgs1 at 29 cM was identified as a potential candidate gene for Abhr2. Sequence analysis of Mrc1 and Ptgs1 sequences did not detect polymorphism between A/J and C3H/HeJ. Gene expression analysis of Mrc1 and Ptgs1 lung mRNA following induction of allergic asthma in A/J and C3H/HeJ animals was performed. Ptgs1 was found to be downregulated in both inbred strains 72 hours after allergic asthma induction; however a strain-specific expression difference was not detected.