作者： Sarkar, P., El-Mohtar, C., Wang, C., Turner, D., Welker, S., Robertson, C. J., Orbović, V., Mou, Z. and Levy, A.
摘要：Huanglongbing (HLB), a devastating citrus disease caused by Candidatus Liberibacter asiaticus (CLas), triggers persistent immune activation marked by excessive callose deposition and reactive oxygen species (ROS) accumulation, which impairs phloem function. This maladaptive response has led to HLB being described as a 'pathogen-triggered immune disease'. Overexpression of the Arabidopsis (Arabidopsis thaliana) NONEXPRESSOR OF PATHOGENESIS-RELATED GENES1 (AtNPR1) gene, a master regulator of systemic acquired resistance (SAR), confers robust HLB tolerance in susceptible citrus varieties, with transgenic lines exhibiting minimal or no disease symptoms following CLas infection. However, the mechanism underlying this tolerance remains unclear. In this study, we demonstrate that AtNPR1 restores immune homeostasis in CLas-infected trees by suppressing callose and ROS hyperaccumulation, thereby alleviating HLB symptom development. Similarly, silencing the Citrus sinensis homolog of NPR3 (CsNPR3), a negative regulator of SAR, mitigates CLas-induced immune overactivation and enhances HLB tolerance. Notably, salicylic acid (SA) levels are lower in AtNPR1-overexpressing citrus plants than wild-type controls after CLas infection, consistent with NPR1's role in negative feedback regulation of pathogen-induced SA accumulation. In Arabidopsis, overexpression of AtNPR1 or disruption of AtNPR3/AtNPR4 also attenuates pathogen-induced callose and ROS responses. Together, these findings reveal conserved roles for NPR1/NPR3/NPR4 in immune regulation across species and suggest that HLB susceptibility in commercial citrus varieties stems from a diminished capacity to maintain immune balance.
文献注录： Sarkar, P., El-Mohtar, C., Wang, C., Turner, D., Welker, S., Robertson, C. J., Orbović, V., Mou, Z. and Levy, A.. NPR1 suppresses Candidatus Liberibacter asiaticus-induced callose and reactive oxygen species accumulation [J]. . 2025.
报/刊名：《》，发表于2025
文献类型： [J]
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