The present studies were carried out to evaluate resistance in the populations of Spodoptera litura Fab. (Lepidoptera, Noctuidae) from five districts of Hunan Province in China to various insecticides from 2010 to 2012 using a standard leaf dip bioassay method. For organophosphates and pyrethroids, resistance ratios compared with a susceptible Lab-BJ strain were in the range of 14–229-fold for organophosphates and 12–227-fold for pyrethroids. Similarly, relative low levels of resistance to emamectin, indoxacarb, and chlorfenapyr were observed in all five populations. In contrast, the resistance to carbamates (thiodicarb or methomyl) was significantly higher than that of organophosphates, pyrethroids and newer chemistry insecticides. The pairwise correlation coefficients of LC₅₀ values indicated that the newer chemistry insecticides and old generation insecticides were not significant except abamectin, which was negatively significantly correlated with methomyl. A significant correlation was observed between thiodicarb, methomyl, and deltamethrin, whereas resistance to bifenthrin showed no correlations with resistance to other insecticides except deltamethrin. The results are discussed in relation to integrated pest management for S. litura with special reference to management of field evolved resistance to insecticides.

The whitefly Bemisia tabaci is an important pest of worldwide agriculture. Previous work has shown that B. tabaci actively suppresses host plant defenses, but our knowledge of the specific mechanisms involved remains limited. Here we describe a B. tabaci salivary protein, the ferritin BtFer1, and its role in facilitating exploitation of host plants. We show that BtFer1 exhibits Fe²⁺ binding ability and ferroxidase activity, and that secretion of BtFer1 during B. tabaci feeding suppresses H₂O₂-generated oxidative signals in tomato (Solanum lycopersicum). Silencing BtFer1 enhanced the induction of the jasmonic acid (JA)-mediated defense signaling pathway in response to whitefly feeding, and led to increased callose deposition and the production of proteinase inhibitors that prevent whiteflies from continuously ingesting and digesting phloem sap. Consistent with these effects, silencing BtFer1 reduced whitefly survival on tomato but not on artificial diet. Using a JA-deficient spr2 mutant plant further showed that suppression of JA defenses by BtFer1 is sufficient to increase B. tabaci survival. Taken together, these results demonstrate that BtFer1 acts as an effector protein that mediates whitefly–tomato interactions. These findings represent an important step forward in understanding the molecular mechanisms by which whiteflies and other insect herbivores suppress host plant defenses.