Biochemical and Molecular Analysis of Field Resistance to Spirodiclofen in Panonychus citri (McGregor).

Previous synergism and enzymatic assays pointed out that CCEs involved spirodiclofen resistance in I T. urticae i , which was subsequently held the involvement of I CCE04 i in spirodiclofen resistance seem more likely to quantitative differences based on kinetic enzyme data [[43]]. The difference in the results obtained in the study of Lv et al. [[67]] and the current study is consistent with spirodiclofen resistance in I T. urticae i [[38]] and I P. ulmi i [[21]], indicating that the spirodiclofen resistance mechanism is complex and may differ among spider mite strains. The level of spirodiclofen resistance in the eggs of this study was different from observations made in I T. urticae i and I P. ulmi i ; eggs from I T. urticae i and I P. ulmi i strains expressing high spirodiclofen resistance in larvae were susceptible to moderate resistance to spirodiclofen [[26], [39]]. Previous studies showed that the inhibitor piperonylbutoxide (PBO) could enhance the toxicity of spirodiclofen in resistant strains ( I T. urticae i , I P. citri i , and I P. ulmi i ), suggesting P450s were involved in spirodiclofen resistance in both tetranychid species [[28], [37], [39]]. Enzymatic assays combined with RNA sequencing results did not indicate the involvement of GST enzymes in the spirodiclofen resistance of I P. citri i , which differs from the results of Lv et al. [[67]], who found that the upregulated GST genes I TuGSTd1 i and I TuGSTd2 i are likely to contribute to spirodiclofen resistance in I T. urticae i . [Extracted from the article]