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Abstract
The mode of action of amitraz is thought to be its toxic effects on a receptor for
a neuromodulator, octopamine. Resistance could arise from modifications of this receptor
so that it would not be affected by amitraz. A putative octopamine receptor cDNA was
cloned and sequenced from a cattle tick in Australia. However, when the sequence was
compared between Australian strains of amitraz-susceptible and resistant ticks, no
differences were detected. We have sequenced this putative octopamine receptor gene
in tick strains from America. The American ticks have a sequence almost identical
to that of the Australian ticks with no deletions or additions in the open reading
frame. In a Brazilian strain and a Mexican strain that are very resistant to amitraz,
there are two nucleotide substitutions that result in amino acids different from all
the susceptible strains. Discovery of these mutations only in amitraz-resistant ticks
provides the first evidence for the possibility of an altered pesticide target site
as a mechanism of amitraz resistance in ticks.