# Protein kinase R-like ER kinase (PERK) is involved in the endoplasmic reticulum stress response of its psyllid vector to Candidatus Liberibacter solanacearum infection

## TL;DR

This study explores how a bacterial pathogen manipulates a psyllid's cellular stress response to aid its transmission.

## Contribution

The study reveals PERK's role in CLso-induced apoptosis and ER stress in psyllids, highlighting species-specific immune responses.

## Key findings

- PERK is activated in CLso-infected psyllid midguts despite reduced gene expression.
- PERK inhibition alters apoptosis-related gene expression in infected psyllids.
- CLso and CLas differentially regulate PERK in their respective psyllid vectors.

## 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.

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.