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ARS Home » Research » Publications at this Location » Publication #102291
Title: IDENTIFICATION OF A POINT MUTATION IN THE PARA-TYPE SODIUM CHANNEL GENE FROM A PYRETHROID-RESISTANT CATTLE TICK

Author
item He, Louis
item Chen, Andrew
item Davey, Ronald
item Ivie, Glen - Wayne
item George, John

Submitted to: Biochemical and Biophysical Research Communications
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/6/1999
Publication Date: N/A
Citation: N/A

Interpretive Summary: Although the southern cattle tick (SCT) and the disease it transmits, babesiosis, were eradicated from the US after a 50-year eradication program of dipping cattle and temporarily vacating tick-infested pastures, these ticks are still widespread in Mexico and other parts of America. Quarantine by vat dipping cattle with chemical pesticides has prevented reinfestation in the US. But SCT has developed resistance to such pesticides. An understanding of mechanisms of pesticide resistance can help develop rapid, sensitive, and accurate methods for detecting resistance, which will lead to better pest management strategies and prolong the usefulness of the currently available pesticides. We investigated whether the mechanism of insect resistance to a certain type of pesticide is responsible for resistance in the SCT. We have found that there are genetic difference in susceptible and resistant ticks and this information will help us design highly sensitive and accurate methods for detecting resistant ticks in the field. This information will help assure that the SCT never again becomes a major threat to cattle producers in this country.

Technical Abstract: To investigate the molecular mechanism of resistance to pyrethroids in the southern cattle tick, Boophilus microplus, we have obtained and sequenced a partial para-homologous sodium channel cDNA from susceptible and pyrethroid resistant tick strains. A point mutation that results in an amino acid change from Phe to Ile was identified in the highly conserved domain IIIS6 of the homologous sodium channel from ticks that are highly resistant to pyrethroid acaricides. This mutation is at a location different from those reported in the same gene in pyrethroid resistant insects.