Main conclusion

Candidate resistance genes encoding malectin-like and LRR domains mapped to halo blight resistance loci throughout the common bean genome are co-expressed to fight a range of Pph races. Common bean (Phaseolus vulgaris L.) is an important crop both as a source of protein and other nutrients for human nutrition and as a nitrogen fixer that benefits sustainable agriculture. This crop is affected by halo blight disease, caused by the bacterium Pseudomonas syringae pv. phaseolicola (Pph), which can lead to 45% yield losses. Common bean resistance to Pph is conferred by six loci (Pse-1 to Pse-6) and minor-effect quantitative trait loci (QTLs); however, information is lacking on the molecular mechanisms implicated in this resistance. Here, we describe an in-depth RNA-sequencing (RNA-seq) analysis of the tolerant G2333 bean line in response to the Pph strain NPS3121. We identified 275 upregulated and 357 downregulated common bean genes in response to Pph infection. These differentially expressed genes were mapped to all 11 chromosomes of P. vulgaris. The upregulated genes were primarily components of plant immune responses and negative regulation of photosynthesis, with enrichment for leucine-rich repeat (LRRs) and/or malectin-like carbohydrate-binding domains. Interestingly, LRRs and malectin genes mapped to the same location as previously identified Pph resistance loci or QTLs. For instance, the major loci Pse-6/HB4.2 involved in broad-resistance to many Pph races co-located with induced LRR-encoding genes on Pv04. These findings indicate a coordinated modulation of genes involved in pathogen perception and signal transduction. In addition, the results further support these LRR/malectin loci as resistance genes in response to halo blight. Thus, these genes are potential targets for future genetic manipulation, enabling the introduction of resistance to Pph into elite cultivars of common bean.

Multiple Salmonella enterica serovars and strains have been reported to be able to persist inside the foliar tissue of lettuce (Lactuca sativa L.), potentially resisting washing steps and reaching the consumer. Intraspecies variation of the bacterial pathogen and of the plant host can both significantly affect the outcome of foliar colonization. However, current understanding of the mechanisms underlying this phenomenon is still very limited. In this study, we evaluated the foliar fitness of 14 genetically barcoded S. enterica isolates from 10 different serovars, collected from plant and animal sources. The S. enterica isolates were vacuum-infiltrated individually or in pools into the leaves of three- to four-week-old lettuce plants. To estimate the survival capacity of individual isolates, we enumerated the bacterial populations at 0- and 10- days post-inoculation (DPI) and calculated their net growth. The competition of isolates in the lettuce apoplast was assessed through the determination of the relative abundance change of barcode counts of each isolate within pools during the 10 DPI experimental period. Isolates exhibiting varying apoplast fitness phenotypes were used to evaluate their capacity to grow in metabolites extracted from the lettuce apoplast and to elicit the reactive oxygen species burst immune response. Our study revealed that strains of S. enterica can substantially differ in their ability to survive and compete in a co-inhabited lettuce leaf apoplast. The differential foliar fitness observed among these S. enterica isolates might be explained, in part, by their ability to utilize nutrients available in the apoplast and to evade plant immune responses in this niche.