Application of rapamycin and evaluate autophagic responses in Bactericera cockerelli

Autophagy is a cellular mechanism of “self-eating”. This catabolic process results in the autophagosomic-lysosomal degradation of bulk cytoplasmic contents, abnormal protein aggregates, and excess or damaged organelles to promote cell survival. According to rapidly expanding data, autophagy is a component of the innate immunity in insects and is involved in the host defense clearance of pathogens, including bacteria. However, little is known about the involvement of autophagy in the interactions of insect vectors with plant bacterial pathogens. The potato psyllid, Bactericera cockerelli, is a native species that transmits the plant bacterial pathogen ‘Candidatus Liberibacter solanacearum’ (Lso). This pathogen causes serious damage to solanaceous crops. Our previous studies showed that autophagy could be involved in the psyllid response to Lso and could affect pathogen acquisition, but the tools to evaluate this response have not been validated in psyllids. Towards this end, the effect of rapamycin, a commonly used autophagy inducer, on potato psyllid survival and the expression of autophagy-related genes was evaluated. Further, autophagic activity was assessed via microscopy and by measure of autophagic flux. Artificial diet-feeding assays using rapamycin resulted in significant psyllid mortality, regulation of autophagy-related genes and increase in autophagic flux, as well as an increased amount of autolysosomes. This study represents a stepping-stone to determine the role of autophagy in psyllid immunity and could be used to develop transmission disruption strategies.