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A Candidatus liberibacter Asiaticus effector, CLIBASIA₀0185 controls sugar metabolism, phenylpropanoid biosynthesis, and endocytosis pathway in Citrus sinensis
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A Candidatus liberibacter Asiaticus effector, CLIBASIA₀0185 controls sugar metabolism, phenylpropanoid biosynthesis, and endocytosis pathway in Citrus sinensis
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Journal Article
A Candidatus liberibacter Asiaticus effector, CLIBASIA₀0185 controls sugar metabolism, phenylpropanoid biosynthesis, and endocytosis pathway in Citrus sinensis
2025
Overview
Citrus Huanglongbing (HLB) is the most catastrophic citrus disease worldwide. SEC-dependent effectors (SDEs) play prominent roles in HLB pathogenesis, and 86 were predicted from the genome of Candidatus Liberibacter asiaticus. Nevertheless, little is known about the comprehensive picture of effector action mechanisms. In this study, RNA-seq was performed to explore the gene expression profiling of transgenic citrus plants expressing a CLas SDE, CLIBASIA₀0185 (0185-OE). A total of 6,506 differentially expressed genes (DEGs) were identified between 0185-OEs and the wild-type (WT) control through RNA-seq. Gene ontology (GO) analysis indicated that molecular functions associated with cellular process, cell part, binding, and catalysis activity were affected. Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis revealed that DEGs were enriched in pathways including primary and secondary metabolisms. Further analysis demonstrated that DEGs implicated in sugar metabolism, phenylpropanoid biosynthesis, and endocytosis pathway were markedly induced in 0185-OE group compared to those in WTs. Ten genes were chosen to verify RNA-seq data with qRT-PCR, and their expression patterns were in good agreement with those of RNA-seq. The transcriptomic analysis demonstrated that CLIBASIA₀0185 (CLas0185) governed sugar metabolism, phenylpropanoid biosynthesis and endocytosis for pathogen survival and development. The results determined a prominent role of CLas0185 in HLB pathogenicity that could be a target for disease management.
Publisher
BioMed Central Ltd,BioMed Central,BMC
Subject
