Association of endoplasmic reticulum associated degradation (ERAD) with the transmission of Liberibacter solanacearum by its psyllid vector.

Abstract

Candidatus Liberibacter solanacearum (CLso) is a complex of gram negative plant pathogenic and fastidious bacterial haplotypes restricted to the phloem and transmitted by several psyllid species. In Israel, the carrot psyllid Bactericera trigonica transmits CLso haplotype D in a persistent and propagative manner and causes the carrot yellows disease, inflicting significant economic losses in many countries. Understanding the transmission of CLso is fundamental to devising sustainable management strategies. Persistent transmission of vector-borne pathogens involves the critical steps of adhesion, cell invasion and replication inside the insect gut cells before passage to the hemolymph. Using microscopy and expression analyses, we have previously confirmed a role for the endoplasmic reticulum (ER) in inducing immune responses and subsequent molecular pathways resulting in programmed cell death (apoptosis) upon CLso-infection in the midgut. In the current study, we confirm that the ER-associated degradation (ERAD) machinery and its associated marker genes were upregulated in CLso infected insects, including Derlin-1, Selenoprotein-1 and Ubiquitin Ligase RNF-185. Silencing Derlin-1, which acts on the ER membrane by regulating the degradation of unfolded proteins upon ER stress, revealed its role in CLso persistence and transmission. Molecular pathways initiated in the ER membrane upon bacterial infection are well documented in human, animal and insect systems, and this study confirms the role of the ER in CLso-psyllid interactions.