Nineteen lines of house flies were derived from crosses of the pyrethroid resistant LPR (wild type) and susceptible aabys (bearing recessive morphological markers on each of five autosomes) strains. Each line was homozygous for one or more wild-type markers from the LPR strain. The level of resistance to permethrin, with and without piperonyl butoxide (PBO), was measured for each line in order to determine the genetic linkage of pyrethroid resistance in LPR house flies. Permethrin resistance in the LPR strain was 16,000-fold compared to the susceptible aabys strain. Resistance in strains bearing wild-type markers for autosomes 1, 2, and 3 together was not significantly different from that of the LPR strain. Resistance in strains bearing a mutant marker for autosomes 1, 2, or 3 (i.e., from aabys) was much lower than in LPR. These results demonstrate that pyrethroid resistance in the LPR strain is polygenic, with genes for resistance on autosomes 1, 2, and 3. PBO decreased permethrin resistance in strains bearing wild-type markers on both autosomes 1 and 2 by 72- to 76-fold, compared to a 78-fold decrease in the LPR strain. However, when the autosome 1 or autosome 2 mutant marker was present, PBO did not substantially decrease the resistance. Thus, the high level of PBO-suppressible resistance in the LPR strain (i.e., P450-mediated detoxication) was associated with autosomes 1 and 2 in combination. The regulation of PBO-suppressible resistance in the LPR strain is discussed. (C) 1995 Academic Press, Inc.