Publications

4461

ABSTRACT Vector-borne transmission of plant and animal pathogens requires active engagement of the vector’s immune system, as pathogens must overcome barriers and exploit host cellular mechanisms. Candidatus Liberibacter solanacearum (CLso) and C. L. asiaticus (CLas) are gram-negative, phloem-limited bacteria transmitted by the psyllids Bactericera trigonica and Diaphorina citri , respectively. Both pathogens induce endoplasmic reticulum (ER) stress and apoptosis in the midguts of their respective vectors, promoting their transmission. The protein kinase R-like endoplasmic reticulum kinase (PERK), a key regulator of ER stress and the unfolded protein response (UPR), plays a crucial role in modulating immunity. In this study, we investigated the role of PERK in CLso-induced apoptosis. PERK expression was downregulated in CLso-infected adult psyllids and midguts, yet immunostaining revealed a significant increase in phosphorylated (active) PERK in infected midguts, despite reduced gene expression. Additionally, ER stress-inducing treatments in both infected and uninfected psyllids demonstrated that CLso infection differentially regulates PERK expression. Interestingly, similar treatments in CLas-infected and uninfected D. citri yielded different results, suggesting species-specific immune responses. Furthermore, inhibition of PERK altered the expression of apoptosis-related genes in CLso-infected psyllids, indicating its involvement in CLso-induced apoptosis. Our findings suggest that PERK and UPR play a role in initiating immune responses at the ER interface in response to CLso, ultimately contributing to apoptosis, which may aid pathogen transmission. While the precise mechanisms by which CLso controls these processes remain unclear, this study provides new insights into how vector-borne plant and potentially animal pathogens manipulate host cellular pathways to enhance their spread. IMPORTANCE This study provides valuable insights into how vector-borne pathogens manipulate host cellular pathways to promote their survival and transmission. Candidatus Liberibacter solanacearum (CLso) and C. L. asiaticus (CLas) cause severe plant diseases, such as zebra chip in potatoes, carrot yellows, and huanglongbing (citrus greening), posing significant threats to global agriculture. By revealing the role of PERK and the unfolded protein response (UPR) in CLso-induced apoptosis, our findings contribute to the growing understanding of insect immunity and pathogen-host interactions. Understanding how CLso influences ER stress and immune signaling in its psyllid vector could lead to innovative strategies to disrupt pathogen persistence and transmission, ultimately supporting disease management efforts.

The X-disease phytoplasma (‘ Candidatus Phytoplasma pruni’) is an obligate pathogen that is capable of infection, persistence, and pathogenicity in both its major plant host ( Prunus spp.) and leafhopper vector ( Colladonus spp.) species. How ‘ Ca. P. pruni’ interacts with its plant and insect hosts, and how it alters its gene expression to do so, is unknown. Therefore, in this study, we conducted comparative RNA sequencing and differential gene expression analysis on ‘ Ca. P. pruni’-infected Prunus avium and Colladonus reductus samples. We found that the phytoplasma altered the expression of approximately 32% of its annotated protein-coding and pseudogenes, including intercellular transporters, proteolytic activity, and membrane structure, as well as upregulating genes associated with potential mobile units when in insect tissues versus in plant tissues. Most notably, differential expression was observed in genes that were identified by in silico analysis as being putative secreted effectors that may play a role in allowing phytoplasma infection and survival in these two very different host systems, as well as inducing X-disease in Prunus spp., which offers targets for control of this damaging pathogen by disrupting phytoplasma–host interactions. [Formula: see text] Copyright © 2026 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license .