| dc.description.abstract | ‘Candidatus Liberibacter solanacearum’ (Lso), is an emerging and serious bacterial pathogen of solanaceous crops, and it can cause very damaging plant diseases (e.g., zebra chip in potatoes). Presently, two haplotypes of Lso (LsoA and LsoB) are present in North America; both are transmitted by potato psyllid, Bactericera cockerelli (Šulc), in a circulative and persistent manner. The psyllid gut is the first organ Lso encounters and could be a barrier for its transmission. However, the molecular mechanisms involved in Lso acquisition and transmission by the potato psyllid are largely unknown. This dissertation aims to understand the molecular interactions between Lso and the potato psyllid at the gut interface. First, the acquisition and transmission of LsoA or LsoB by potato psyllid were investigated. Second, I investigated the global transcriptional responses of the adult psyllid gut upon infection of the two Lso haplotypes using Illumina sequencing. Third, I explored whether any of these two Lso haplotypes triggered an apoptotic or autophagic response in the gut of the adult potato psyllid. The results indicated that LsoB relative abundance increased faster in the psyllid gut than that of LsoA, and LsoB had a shorter latent period than LsoA. In addition, the transcriptome analyses showed that each haplotype triggers a unique transcriptional response, with most of the distinct gene expression changes being elicited by the highly virulent LsoB. Furthermore, Lso might repress the apoptotic response in the adult psyllid gut by inducing the anti-apoptotic gene IAPP5.2 at the early stage of the infection, which may favor Lso acquisition and colonization of the psyllid gut cells. However, Lso might induce an autophagic response in the adult psyllid gut since the majority of autophagy-related genes (ATGs) are sensitive and responsive to the exposure or infection of both LsoA and LsoB. Further investigation needs to be conducted to deepen the study of autophagic response of potato psyllid to Lso infection. This dissertation is therefore an important contribution to a mechanistic understanding of Lso transmission, provides insights into understanding the adaptive significance of the immune response and has the potential to create new approaches for disrupting Lso transmission. | en |
