|LIU, XU GAN|
|Zhu, Yu Cheng|
Submitted to: Pest Management Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/13/2008
Publication Date: 2/10/2009
Citation: Wang, Y., Liu, X., Zhu, Y., Zhou, W., Shen, J. 2009. Inheritance Mode and Realized Heritability of Resistance to Imidacloprid in the Brown Planthopper, Nilaparvata lugens (Stal) (Homoptera: Delphacidae). Pest Management Science. 65:629-634.
Interpretive Summary: The success of insecticide resistance management strategies depends on a variety of factors, including the clarification of the mode of resistance inheritance. An improved understanding of the genetics of resistance enhances the ability to design and apply resistance management programs, such as facilitating formulation of strategies to slow down the development of imidacloprid resistance in the brown planthopper. Information about the mode of inheritance of resistance to an insecticide can improve resistance detection, monitoring, risk assessment, modeling, and management of the resistance. Because imidacloprid is a relative new insecticide, the genetic basis of resistance in the brown planthopper has not yet been documented. This study was designed to elucidate the mode of inheritance and estimate the realized heritability of imidacloprid resistance in the brown planthopper. Inheritance patterns were examined to determine the degree of dominance of the resistance, possible sex linkages, and the monogenic or polygenic nature of the resistance. Our data are valuable for understanding the resistance and for formulating resistance management strategies.
Technical Abstract: BACKGROUND: The brown planthopper, Nilaparvata lugens (Stål) is a serious pest which 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 laboratory population of N. lugens collected from a rice field near Nanjing, Jiangsu province, China, showed a 964-fold resistance compared with the laboratory strain. Progenies of reciprocal crosses (F1 and F1') showed similar dose-mortality responses (LC50) to imidacloprid, and also exhibited a similar degree of dominance (D), 0.58 for F1 and 0.63 for F1', respectively. Chi-square analyses of self-bred and back-cross progenies (F2, F2', and BC, respectively) rejected the hypothesis for a single gene control of the resistance. The estimated realized heritability (h2) 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.