|Wang, Ruiwu - MICHIGAN STATE UNIVERSITY|
|Dong, Ke - MICHIGAN STATE UNIVERSITY|
|Huang, Zachary - MICHIGAN STATE UNIVERSITY|
Submitted to: Journal of Apicultural Research
Publication Type: Proceedings
Publication Acceptance Date: September 4, 2001
Publication Date: N/A
Interpretive Summary: The varroa mite, Varroa jacobsoni, has developed widespread resistance to the pyrethroid fluvalinate, the standard product for treating infestations in honey bee colonies over the past ten years. Such resistance may be due to greater metabolism within the resistant mite, or, as we investigate here, a change in the genetic locus at the site of action of the pesticide within the mite nervous system. At this time, no modifications in the locus site were detected. We intend to modify test procedures in order to further explore the mechanism of resistance in varroa.
Technical Abstract: Previous genetic and pharmacological studies suggest that reduced target site sensitivity to pyrethroids is an important resistance mechanism. Due to intensive use of fluvalinate, varroa mite (Varroa jacobsoni) recently developed resistance to fluvalinate. To investigate the molecular mechanism of resistance to fluvalinate in varroa mite, we have cloned and sequenced a cDNA fragment of mite para homologous sodium channel gene from susceptible and resistant mite populations. The deduced amino acid sequence of domain II to C terminus of the mite para homologous sodium channel protein shares 66.5%, 49.7%, and 44.4% identity with the para- homolog of the cattle tick (Boophilus microplus) and Drosophila melanogaster, and rat brain type II sodium channel a-subunit respectively. Comparison of the deduced amino acid sequence obtained from five (2 susceptible, 3 resistant) mite populations revealed 8 amino acid differences. However kdr or super-kdr mutation was not detected in any of the three resistant mite populations. In the future, we plan to do better toxicological screening to separate the mites carrying homozygous resistance genes from those that are heterozygous. We will also examine fluvalinate sensitivity of mite wild type and mutant sodium channels expressed in Xenopus oocyte. This would allow us to pin down any mutations that confer fluvalinate resistance in mites. It is our hope that once such mutations are identified, we can use molecular methods such as polymerase chain reaction to survey for resistant genes in mites sampled from honey bee colonies.