Abstract
Huanglongbing (HLB) in citrus infected by Candidatus Liberibacter asiaticus (CLas) has caused tremendous losses to the citrus industry. No resistant genotypes have been identified in citrus species or close relatives. Among citrus varieties, rough lemon (Citrus jambhiri) has been considered tolerant due to its ability to produce a healthy flush of new growth after infection. The difference between tolerance and susceptibility is often defined by the speed and intensity of a plant’s response to a pathogen, especially early defense responses. RNA-seq data were collected from three biological replicates of CLas- and mock-inoculated rough lemon and sweet orange at week 0 and 7 following infection. Functional analysis of the differentially expressed genes (DEGs) indicated that genes involved in the mitogen activated protein kinase (MAPK) signaling pathway were highly upregulated in rough lemon. MAPK induces the transcription of WRKY and other transcription factors which potentially turn on multiple defense-related genes. A Subnetwork Enrichment Analysis further revealed different patterns of regulation of several functional categories, suggesting DEGs with different functions were subjected to reprogramming. In general, the amplitude of the expression of defense-related genes is much greater in rough lemon than in sweet orange. A quantitative disease resistance response may contribute to the durable tolerance level to HLB observed in rough lemon.
Highlights
Huanglongbing (HLB) or citrus greening is one of the most destructive plant diseases in the world.[1]
Even after 8 months, rough lemon did not exhibit any signs of growth inhibition, and continued growth of new shoots with few or no symptoms was observed; the typical blotchy mottled appearance was commonly found on mature, older leaves (Figure 1)
Our study indicates that WRKY transcription factor genes may play an important role in the tolerance to HLB exhibited by rough lemon
Summary
Huanglongbing (HLB) or citrus greening is one of the most destructive plant diseases in the world.[1]. It is generally recognized that after infection or inoculation, CLas bacteria migrate through the phloem and accumulate there, resulting in the formation of sieve plugs, which contribute to HLB symptoms.[3]. Plants have evolved two layers of immune systems, pathogen-associated (or microbe-associated) molecular patterns (PAMP)-triggered immunity (PTI) and effectortriggered immunity. PTI is mediated by pattern-recognition receptors (PRRs) that recognize PAMPs, whereas effectortriggered immunity is mediated by resistance (R) proteins that recognize pathogen effectors.[5]. The role of these immunity systems in citrus greening disease and the transcriptomic response of citrus is poorly understood, especially in regards to the early defense response of rough lemon to HLB infection
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