The stability and biochemical basis of fufenozide resistance in a laboratory-selected strain of Plutella xylostella

Fufenozide, a novel non-steroidal ecdysone agonist, exhibits good efficacy and plays an important role in controlling lepidopteran pests in China. A high level of resistance to fufenozide (320.3-fold) in Plutella xylostella (L.) has been selected under laboratory conditions. In this study, the stability and biochemical basis of resistance to fufenozide were investigated. The resistance ratio to fufezonide declined substantially from 320.3- to 20.5-fold in the fufenozide resistant strain (JSR) when the selection pressure was removed for six consecutive generations. However, the susceptibility to fufezonide could not be fully restored after 28 generations without exposure to the compound. Increased relative fitness (0.87) was associated with the rapid reversal of resistance in the resistance decaying strain (JSRD). The enzymatic analyses showed reduced specific activities of monooxygenase (MO), glutathione S-transferases (GSTs), carboxylesterase and aryl-acylamidase in the JSRD strain, whereas the activity of chitinase increased. The current findings suggest the selected resistance to fufenozide in P. xylostella is not stable, and the four detoxifying enzymes including MO, GSTs, carboxylesterase, and aryl-acylamidase may be involved. For resistance management proposes, insecticide rotation should be a viable option to delay the occurrence of fufenozide resistance in the field.

The resistance to fufenozide in Plutella xylostella decreased quickly and then stabilized at a lower level after the selection pressure was removed.Figure optionsDownload as PowerPoint slideHighlights
► The resistance to the fufenozide in the DBM is not stable at high level.
► Relative fitness of resistant strain was lower than that of the susceptible one.
► Four detoxifying enzymes were involved in the fufenozide resistance in the DBM.