Selection pressure designed to produce 50% mortality was applied to alternate generations of
T. kanzawai, using dicofol and phenthoate on adults and chlordimeform on eggs. The development of resistance was relatively slow in the initial period in chlordimeform-selected and phenthoate-selected strains, and very rapidly intensified resistance and increasing slope were clearly observed with each succeeding generation. On the other hand, the development of resistance in the dicofol-selected strain was almost unchanged through ten generations, and the resistance developed slowly with succeeding generations. Therefore, the number of treatments required to develop resistance in these strains varied with the acaricides used. Adults of resistant strains were crossed with susceptible reference strains, and the F
1 and backcross were tested for resistance. There was little difference between the composition of the F
1 reciprocal crosses or between the backcrosses derived from them, and they partitioned into a 1:1 ratio of resistant and susceptible phenotypes in the backcross. The resistances of these acaricides were considered to be due to a single, incompletely dominant autosomal gene in the case of chlordimeform and phenthoate, and to an incompletely recessive autosomal gene in the case of dicofol.
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