Abstract
A field population of Chrysoperla carnea was exposed for 17 generations to chlorfenapyr insecticide that resulted in 217-fold resistance compared to a susceptible strain. The overlapping of LC50 values in reciprocal crosses and their dominance values indicated that chlorfenapyr resistance was autosomal and incompletely dominant. The chi-square analysis of back-cross mortality confirmed the polygenic nature of chlorfenapyr resistance. The results of effective dominance of chlorfenapyr resistance indicated that resistance at the highest concentration was completely recessive. The realized heritability of chlorfenapyr resistance in the first 9, last 9, and a total of 18 generations was 0.28, 0.42, and 0.31, respectively. Furthermore, synergism results showed that both experimental synergists, PBO and DEF, did not synergize the toxicity of chlorfenapyr. In conclusion, C. carnea had been found to have autosomal, partially dominant, and polygenic chlorfenapyr resistance. Meaning that thereby resistance is inherited through multiple genes and is not limited to a single gene or sex-linked trait. These findings will help to develop an effective IPM model focusing on the simultaneous use of selective insecticides and resistant biocontrol agents to reduce the problem of resistance development in pest populations.
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