|Zhu, Yu Cheng|
Submitted to: Pest Management Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/18/2009
Publication Date: 5/20/2009
Citation: Jia, B., Liu, X., Liu, Y., Zhu, Y., Gao, C., Shen, J. 2009. Inheritance, Fitness Cost, and Mechanism of Resistance to Tebufenozide in Spodoptera exigua (Hubner) (Lepidoptera: Noctuidae). Pest Management Science. 65(9):996-1002
Interpretive Summary: The beet armyworm is a worldwide pest of many important crops, such as vegetables and cotton. Tebufenozide, a novel synthetic non-steroidal ecdysteroid agonist, have been used to control the beet armyworm for more than 10 years. Although laboratory selection suggested that beet armyworm had the potential to develop high level of resistance to tebufenozide, information concerning the mode of resistance inheritance has not been available yet. This study focused mainly on examination of inheritance and fitness cost of tebufenozde resistance in the beet armyworm. In addition, synergistic effects of three enzymatic inhibitors were also evaluated for understanding tebufenozide resistance. The information generated from this study is valuable for understanding resistance development and for designing technique to manage the resistance.
Technical Abstract: BACKGROUND: The efficacy of tebufenozide against the beet armyworm, Spotoptera exigua (Hübner), apparently decreased in recent years. To develop better resistance management strategy, this study was focused on the inheritance and fitness cost of tebufenozide resistance in S. exigua. RESULTS: After being selected with tebufenozide for 74 generations, S. exigua developed 92-fold resistance to the chemical. The degrees of dominance for the reciprocal cross progeny were -0.2651 and -0.2773. The resistant strain had a relative fitness of 0.71 with substantially lower rates of larval survival, pupal weight, pupation, oviposition per female, and prolonged larval and pupal duration. PBO significantly increased toxicity of tebufenozide (SR=1.9) against resistant insects, while DEM and DEF didn’t significantly synergize tebufenozide. CONCLUSION: Tebufenozide resistance in S. exigua was inherited as autosomal, incompletely recessive, and controlled by more than one gene. Development of the resistance may cost significant fitness for the resistant population. Mixed-function oxidase might play an important role in tebufenozide resistance in S. exigua.