Wei Zhang1,2, Nemat O Keyhani1,2, Hao Zhang1, Kaiyong Cai3, Yuxian Xia1. 1. School of Life Sciences, Chongqing Engineering Research Center for Fungal Insecticides, Chongqing University, Chongqing, China. 2. Department of Microbiology and Cell Science, University of Florida, Gainesville, FL, USA. 3. Bioengineering College of Chongqing University, Chongqing, China.
Abstract
BACKGROUND: Environmentally friendly insect management technologies, including RNA interference (RNAi) and entomopathogenic fungi, have attracted increasing attention as options for pest control. Here, we sought to extend RNAi-directed targeting of the inhibitor of apoptosis protein 1 (IAP1) gene to the locust, and to examine its relationship to immune responses and susceptibility to Metarhizium acridum, a locust-specific fungal pathogen. RESULTS: Expression of the locust LmIAP gene was induced in the hemolymph and fat body after M. acridum infection. RNAi-directed silencing of locust LmIAP1 resulted in increased caspase 3 activity, degeneration of the gut and dose-dependent mortality. Synergistic mortality was seen in RNAi-LmIAP/fungal co-infection experiments with median survival time (MST) values decreasing from ∼ 5 days for RNAi and M. acridum treatments alone, to 2.6 days for co-treatments. Reduced hemocyte numbers and antimicrobial peptide levels were seen in co-treated locusts, with changes in gut opportunistic pathogenic bacteria seen between treatments. Enhanced fungal sporulation on co-treated insect cadavers was also compared with fungal infection alone. CONCLUSIONS: Silencing of the locust LmIAP1 gene results in direct mortality and increases insect susceptibility to insect fungal pathogens, in part by decreasing immunity and altering the gut microbiome.
BACKGROUND: Environmentally friendly insect management technologies, including RNA interference (RNAi) and entomopathogenic fungi, have attracted increasing attention as options for pest control. Here, we sought to extend RNAi-directed targeting of the inhibitor of apoptosis protein 1 (IAP1) gene to the locust, and to examine its relationship to immune responses and susceptibility to Metarhizium acridum, a locust-specific fungal pathogen. RESULTS: Expression of the locust LmIAP gene was induced in the hemolymph and fat body after M. acriduminfection. RNAi-directed silencing of locust LmIAP1 resulted in increased caspase 3 activity, degeneration of the gut and dose-dependent mortality. Synergistic mortality was seen in RNAi-LmIAP/fungal co-infection experiments with median survival time (MST) values decreasing from ∼ 5 days for RNAi and M. acridum treatments alone, to 2.6 days for co-treatments. Reduced hemocyte numbers and antimicrobial peptide levels were seen in co-treated locusts, with changes in gut opportunistic pathogenic bacteria seen between treatments. Enhanced fungal sporulation on co-treated insect cadavers was also compared with fungal infection alone. CONCLUSIONS: Silencing of the locust LmIAP1 gene results in direct mortality and increases insect susceptibility to insect fungal pathogens, in part by decreasing immunity and altering the gut microbiome.