Serratia marcescens induces apoptosis in Diaphorina citri gut cells via reactive oxygen species‐mediated oxidative stress

Abstract

AbstractBACKGROUNDAsian citrus psyllid, Diaphorina citri, is a notorious pest in the citrus industry because it transmits Candidatus Liberibacter asiaticus, which causes an uncurable, devastating disease in citrus worldwide. Serratia marcescens is widely distributed in various environments that exhibits toxic effects to many insects. To develop strategies for enhancing the efficiency of pathogen‐induced host mortality, a better understanding of the toxicity mechanism of Serratia marcescens on Diaphorina citri is critical.RESULTSSerratia marcescens KH‐001 successfully colonized Diaphorina citri gut by feeding artificial diets, resulting in the damage of cells including nucleus, mitochondria, vesicles, and microvilli. Oral ingestion of Serratia marcescens KH‐001 strongly induced apoptosis in gut cells by enhancing levels of Cyt c, p53 and caspase‐1 and decreasing levels of inhibitors of apoptosis (IAP) and Bax inhibitor‐1 (BI‐1). The expression of dual oxidase (Duox) and nitric oxide synthase (Nos) was up‐regulated by Serratia marcescens KH‐001, which increased hydrogen peroxide (H2O2) levels in the gut. Injection of abdomen of Diaphorina citri with H2O2 accelerated the death of the adults and induced apoptosis in the gut cells by activating Cyt c, p53 and caspase‐1 and suppressing IAP and BI‐1. Pretreatment of infected Diaphorina citri with vitamin c (Vc) increased the adult survival and diminished the apoptosis‐inducing effect.CONCLUSIONSThe colonization of Serratia marcescens KH‐001 in the guts of Diaphorina citri increased H2O2 accumulation, leading to severe changes and apoptosis in intestinal cells, which enhanced a higher mortality level of D. citr. This study identifies the underlying virulence mechanism of Serratia marcescens KH‐001 on Diaphorina citri that contributes to a widespread application in the integrated management of citrus psyllid. © 2023 Society of Chemical Industry.