BACKGROUND: The brown planthopper, Nilaparvata lugens (Stål), is a serious pest that causes enormous losses to the rice crop in Asia. The genetic basis of imidacloprid resistance was investigated in N. lugens. RESULTS: The resistant strain, selected for imidacloprid resistance from a field population of N. lugens collected from Nanjing, Jiangsu Province, China, showed a 964-fold resistance compared with the laboratory strain. Progenies of reciprocal crosses (F(1) and F(1)') showed similar dose-mortality responses (LC(50)) to imidacloprid, and also exhibited a similar degree of dominance (D), 0.58 for F(1) and 0.63 for F(1)'. Chi-square analyses of self-bred and backcross progenies (F(2), F(2)' and BC respectively) rejected the hypothesis for a single gene control of the resistance. The estimated realized heritability (h(2)) of imidacloprid resistance was 0.1141 in the resistant strain of N. lugens. CONCLUSION: The results showed that imidacloprid resistance in N. lugens was autosomal and was expressed as an incompletely dominant trait, probably controlled by multiple genes.
BACKGROUND: The brown planthopper, Nilaparvata lugens (Stål), is a serious pest that causes enormous losses to the rice crop in Asia. The genetic basis of imidacloprid resistance was investigated in N. lugens. RESULTS: The resistant strain, selected for imidacloprid resistance from a field population of N. lugens collected from Nanjing, Jiangsu Province, China, showed a 964-fold resistance compared with the laboratory strain. Progenies of reciprocal crosses (F(1) and F(1)') showed similar dose-mortality responses (LC(50)) to imidacloprid, and also exhibited a similar degree of dominance (D), 0.58 for F(1) and 0.63 for F(1)'. Chi-square analyses of self-bred and backcross progenies (F(2), F(2)' and BC respectively) rejected the hypothesis for a single gene control of the resistance. The estimated realized heritability (h(2)) of imidacloprid resistance was 0.1141 in the resistant strain of N. lugens. CONCLUSION: The results showed that imidacloprid resistance in N. lugens was autosomal and was expressed as an incompletely dominant trait, probably controlled by multiple genes.