Juvenile hormone-regulated ribosomal protein DcRPS25 Mediates tolerance to Huanglongbing pathogen in the Vector...

Insect vectors often evolve disease tolerance to sustain fitness while harboring high pathogen loads, a strategy critical for the transmission of persistent pathogens. However, the regulatory networks that coordinate the physiological trade-offs required for this tolerant state remain largely unknown. Here, we identify the juvenile hormone (JH)-regulated ribosomal protein DcRPS25 as a critical mediator of pathogen tolerance in the Asian citrus psyllid, Diaphorina citri, the vector of the devastating citrus Huanglongbing pathogen Candidatus Liberibacter asiaticus (CLas). Mechanistically, we show that CLas infection exploits the host endocrine system to elevate JH signaling, which in turn transcriptionally upregulates DcRPS25. Acting as a downstream effector, the JH-driven accumulation of DcRPS25 suppresses reactive oxygen species (ROS)-dependent immune activation. Simultaneously, it sustains essential host translation for reproductive fitness, thereby establishing an immunocompromised yet high-fitness niche that is permissive for CLas proliferation. Disruption of this axis collapses tolerance: DcRPS25 knockdown reduces CLas burden but paradoxically compromises host survival under infection. Leveraging this mechanism, we engineer a chitosan-based dsRNA nanopesticide targeting DcRPS25. This formulation effectively suppresses vector populations and blocks pathogen transmission without harming beneficial insects. Our findings unveil a novel "Endocrine-Ribosome-Immunity" axis underlying vector competence and demonstrate the translational potential of disrupting tolerance mechanisms for sustainable disease management.