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Rikkerink, E. H. A.

Publications and source records attributed to Rikkerink, E. H. A..

2 recordsLinked to original sources

Re-programming of Pseudomonas syringae pv. actinidiae gene expression during early stages of infection of kiwifruit

BackgroundPseudomonas syringae is a widespread bacterial species complex that includes a number of significant plant pathogens. Amongst these, P. syringae pv. actinidiae (Psa) initiated a worldwide pandemic in 2008 on cultivars of Actinidia chinensis var. chinensis. To gain information about the expression of genes involved in pathogenicity we have carried out transcriptome analysis of Psa during the early stages of kiwifruit infection.\n\nResultsGene expression in Psa was investigated during the first five days after infection of kiwifruit plantlets, using RNA-seq. Principal component and heatmap analyses showed distinct phases of gene expression during the time course of infection. The first phase was an immediate transient peak of induction around three hours post inoculation (HPI) that included genes that code for a Type VI Secretion System and nutrient acquisition (particularly phosphate). This was followed by a significant commitment, between 3 and 24 HPI, to the induction of genes encoding the Type III Secretion System (T3SS) and Type III Secreted Effectors (T3SE). Expression of these genes collectively accounted for 6.3% of the bacterial transcriptome at this stage. There was considerable variation in the expression levels of individual T3SEs but all followed the same temporal expression pattern, with the exception of HopAS1, which peaked later in expression at 48 HPI. As infection progressed over the time course of five days, there was an increase in the expression of genes with roles in sugar, amino acid and sulfur transport and the production of alginate and colanic acid. These are both polymers that are major constituents of extracellular polysaccharide substances (EPS) and are involved in biofilm production. Reverse transcription-quantitative PCR (RT-qPCR) on an independent infection time course experiment showed that the expression profile of selected bacterial genes at each infection phase correlated well with the RNA-seq data.\n\nConclusionsThe results from this study indicate that there is a complex remodeling of the transcriptome during the early stages of infection, with at least three distinct phases of coordinated gene expression. These include genes induced during the immediate contact with the host, those involved in the initiation of infection, and finally those responsible for nutrient acquisition.

microbiology

NRG1-mediated recognition of HopQ1 reveals a link between PAMP and Effector-triggered Immunity.

O_LIMembers of the hopQ1/XopQ family of effectors are conserved amongst pathogenic bacteria suggesting an important function in virulence. Therefore, the identification of R proteins recognising members of this family is potentially of high value to achieve broad-spectrum resistance in crops.\nC_LIO_LIRecent studies demonstrated that HopQ1/XopQ recognition is EDS1-dependant and is mediated by the TIR-NB-LRR protein Roq1. Using our recently described R gene RNAi library, we have investigated the mechanism of HopQ1 recognition and the other components of its signalling network.\nC_LIO_LIWe show that silencing of the CCR-NB-LRR helper protein N Requirement Gene 1 (NRG1) prevents HopQ1 recognition in N. benthamiana and that NRG1 expression confers recognition of HopQ1 and restricts Pto DC3000 proliferation in the otherwise susceptible host Arabidopsis. Moreover NRG1 expression is briefly but strongly induced at a very early stage of the plant innate response, establishing a strong dependency link between PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI).\nC_LIO_LIOverall we demonstrate that in addition to Roq1, HopQ1 recognition in N. benthamiana requires the CCR-NB-LRR protein NRG1 and propose a model based on the dual requirement of a CCR-NB-LRR and a TIR-NB-LRR that could extend beyond HopQ1 detection and possibly be used to recognize other pathogen effectors.\nC_LI

plant biology