Airway hyperresponsiveness is a key characteristic of human asthma and
a marker for asthma-like conditions in animals. F-1 mice derived from
A/J and C57BL/6J display a phenotype which resembles the asthma-like
phenotype of the A/J mice. Since airway responsiveness failed to segre
gate as a mendelian trait, we show significant linkage at two loci, Bh
r1 (lod = 3.0) and Bhr2 (lod = 3.7) on chromosomes 2 and 15. A third l
ocus, Bhr3 (lod = 2.83), maps to chromosome 17. Each of these loci map
s near candidate loci implicated in the pathobiology of asthma. Our st
udy represents the first linkages established through a genome-wide su
rvey of airway hyperresponsiveness in any mammal.