ORIGINAL RESEARCH article
Front. Plant Sci.
Sec. Plant Pathogen Interactions
This article is part of the Research TopicUnraveling Molecular Mechanisms of Citrus Resistance to HuanglongbingView all 7 articles
Early Tolerance Mechanisms in Citrus: Transcriptome and Hormone Profiling of NPR1-Mediated Responses to Candidatus Liberibacter asiaticus
Provisionally accepted
- 1University of California Riverside, Riverside, United States
- 2Department of Plant Pathology, University of Florida, Gainesville, United States
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Huanglongbing (HLB), caused by Candidatus Liberibacter asiaticus (CLas), is the most destructive citrus disease worldwide, severely reducing yield and fruit quality. Although no naturally resistant cultivars are available, citrus plants overexpressing Arabidopsis NPR1 (AtNPR1) display enhanced tolerance, yet the molecular mechanisms underlying this phenotype remain insufficiently understood. To uncover early transcriptional events associated with tolerance, we performed comparative RNA-seq and phytohormone profiling of susceptible wild-type (WT) and tolerant AtNPR1-overexpressing (AtNPR1-OE) Duncan grapefruit at 0, 6, and 24 hours post infection (hpi). Before infection, AtNPR1 plants downregulated genes involved in cytoskeleton organization, cell wall biogenesis, and receptor signaling, suggesting a primed basal defense state. After CLas exposure, AtNPR1 plants exhibited stronger and earlier transcriptional reprogramming, with substantially more differentially expressed genes at 6 hpi than WT. At 24 hpi, AtNPR1 plants showed suppression of callose synthase genes and selective induction of β-1,3-glucanases, indicating more controlled phloem callose regulation. Concurrently, attenuated expression of respiratory burst oxidase homologs and ROS-associated genes suggested a moderated and less damaging oxidative burst. Hormone measurements further supported a coordinated defense adjustment. AtNPR1 plants maintained stable levels of salicylic acid, and gibberellins while preventing the infection-drivenCLas-induced rise ininduction of abscisic acid observed in WT. Collectively, these findings reveal that AtNPR1 overexpression enhances HLB tolerance by integrating early transcriptional reprogramming with balanced structural, oxidative, and hormonal responses. This study provides a mechanistic framework for understanding NPR1-mediated tolerance to CLas during the initial stages of infection.
Keywords: Liberibacter, Citrus, NPR1, Transcriptome, Immunity
Received: 06 Oct 2025; Accepted: 05 Dec 2025.
Copyright: © 2025 Sarkar, Wang and Levy. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Poulami Sarkar
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