|Authors: ||V. Michelotti, A. Lamontanara, L. Orrų, G. Buriani, I. Donati, L. Fiorentini, G. Tacconi, F. Spinelli|
|Keywords: ||Pseudomonas syringae pv. actinidiae, differentially expressed genes, RNA-seq|
Pseudomonas syringae pv. actinidiae (Psa), the causal agent of bacterial canker of kiwifruit, was first isolated in 1989. A pandemic outbreak that started in 2008 is seriously threatening kiwifruit production worldwide.
Very little is known about the molecular mechanisms involved in this host-pathogen interaction.
In this study, an RNAseq approach was applied to identify the virulence genes of Psa involved in pathogenicity.
Transcriptome analysis was carried out on Psa grown in LB medium (PsaLB) or in LB medium supplemented with plant extracts of Actinidia deliciosa (PsaAd) or Actinidia chinensis (PsaAc). Differential gene expression analysis under all three tested conditions highlighted widespread transcriptional modulation, with up to 2000 genes listed as significantly differentially expressed genes (DEGs), which represents about half of the total number of Psa genes.
Many of the genes found to be upregulated in Psa cells exposed to plant extracts were involved in functions such as motility, chemotaxis, adherence and iron acquisition, which are functions associated with plant colonization.
However, under the PsaAd and PsaAc conditions, genes coding for the type-III secretion system and type-III effector proteins, which are known to be essential for virulence of P. syringae, were downregulated.
These data suggest that regulation of the expression of type-III secretion system genes was dependent on plant signals distinct from those that control expression of genes involved in motility, and invasion and might require direct interaction with plant cells in intact tissue.
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