Please use this identifier to cite or link to this item: https://hdl.handle.net/1959.11/27922
Title: Buprofezin Resistance in B-biotype Bemisia tabaci
Contributor(s): Cottage, Emma Louise Ariel (author); Gunning, Robin (supervisor); Gregg, Peter  (supervisor)orcid 
Conferred Date: 2003-10-11
Open Access: Yes
Handle Link: https://hdl.handle.net/1959.11/27922
Abstract: Laboratory selection of an Australian B-biotype Bemisia tabaci population with the insect growth regulator buprofezin rapidly produced high levels of buprofezin resistance (in excess of 2000-fold) after 4 applications. An unselected B-biotype B. tabaci population was originally 11-fold resistant to buprofezin. mechanism studies showed two mechanisms of resistance.
Buprofezin resistant B-biotype B. tabaci had higher esterase activity and additional esterase bands compared to a buprofezin unselected B-biotype and native Australian non B-biotype B. tabaci strains. Esterase from buprofezin resistant B-biotype B. tabaci was inhibited both in vitro and in vivo by buprofezin to a far greater degree (2- fold) than in the non buprofezin selected B. tabaci strain. Esterase from insecticide susceptible native non B-biotype B. tabaci and SUD-S strains was uninhibited by buprofezin. Esterase mediated sequestration of buprofezin is proposed as a mechanism of resistance to buprofezin in B. tabaci. This is the first report of a resistance mechanism to buprofezin in B. tabaci.
Other insecticides with novel modes of action were investigated for effects on B. tabaci esterases. Pyriproxyfen inhibited esterase activity in vitro in both resistant and non selected B-biotype strains and this implied cross-resistance was confirmed by bioassay. Novaluron and pymetrozine also inhibited esterase in buprofezin resistant B. tabaci, but not in the unselected population. Fenoxycarb did not inhibit esterase activity in either strain.
Acetylcholinesterase (AChE) studies showed a new mode of action for IGRs and a second buprofezin resistance mechanism. Buprofezin resistant B-biotype B. tabaci AChE had a different electrophoretic mobility to both the unselected and non Bbiotype strains. Buprofezin inhibited AChE activity in the non selected B-biotype population, but not in resistant B. tabaci. The mutant form of AChE in B-biotype B. tabaci appeared to be unrelated to previously discovered AChE variants.
Results also showed that another IGR (novaluron) inhibited AChE activity in nonbuprofezin selected strain, but buprofezin resistant AChE was unaffected. Experiments indicated no significant differences in mono-oxygenase activity in either the buprofezin unselected or resistant B. tabaci strains.
The speed with which B. tabaci were selected for high levels of buprofezin resistance, and the potential for cross-resistance between insect growth regulators is a warning that buprofezin should be used sparingly against B. tabaci and in rotation with other insecticides. The results have already provided essential information for the whitefly insecticide resistance management strategy in central Queensland. With the escalating problem of B-biotype B. tabaci in many Australian crop production systems, including cotton, an effective management strategy is vital.
Publication Type: Thesis Doctoral
HERDC Category Description: T2 Thesis - Doctorate by Research
Appears in Collections:School of Environmental and Rural Science
Thesis Doctoral

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