Pseudomonas syringae pv. syringae is the main causal agent of bacterial canker in sweet cherry in Chile, causing significant economic losses. Cultivars exhibit diverse susceptibility in the field and the molecular mechanisms underlying the differential responses remain unclear. RNA-seq analysis was performed to characterize the transcriptomic response in cultivars Santina and Bing (less and more susceptible to P. syringae pv. syringae, respectively) after 1 and 7 days post-inoculation (dpi) with the bacterium. Symptoms of bacterial canker became evident from the fifth day. At 1 dpi, cultivar Santina showed a faster response to infection and a larger number of differentially expressed genes (DEGs) than cultivar Bing. At 7 dpi, cultivar Bing almost doubled its DEGs, while cultivar Santina tended to the normal DEG levels. P. syringae pv. syringae infection downregulated the expressions of key genes of the photosynthesis process at 1 dpi in the less susceptible cultivar. The results suggest that the difference in susceptibility to P. syringae pv. syringae is linked to the timeliness of pathogen recognition, limiting the bacteria’s dispersion through modeling its cell wall, and regulation of genes encoding photosynthesis pathway. Through this study, it has been possible to progress the knowledge of relevant factors related to the susceptibility of the two studied cherry cultivars to P. syringae pv. syringae.

Bacterial canker caused by Pseudomonas syringae pv. syringae (Pss) is responsible for substantial loss to the production of sweet cherry in Chile. To date, the molecular mechanisms of the Pss–sweet cherry interaction and the disease-related genes in the plant are poorly understood. In order to gain insight into these aspects, a transcriptomic analysis of the sweet cherry cultivar ‘Lapins’ for differentially expressed genes (DEGs) in response to Pss inoculation was conducted. Three Pss strains, A1M3, A1M197, and 11116_b1, were inoculated in young twigs, and RNA was extracted from tissue samples at the inoculation site and distal sections. RNA sequencing and transcriptomic expression analysis revealed that the three strains induced different patterns of responses in local and distal tissues. In the local tissues, A1M3 triggered a much more extensive response than the other two strains, enriching DEGs especially involved in photosynthesis. In the distal tissues, the three strains triggered a comparable extent of responses, among which 11116_b1 induced a group of DEGs involved in defense responses. Furthermore, tissues from various inoculations exhibited an enrichment of DEGs related to carbohydrate metabolism, terpene metabolism, and cell wall biogenesis. This study opened doors to future research on the Pss–sweet cherry interaction, immunity responses, and disease control.

Disease severity and drought due to climate change present significant challenges to orchard productivity. This study examines the effects of spring inoculation with Pseudomonas syringae pv. syringae (Pss) on sweet cherry plants, cvs. Bing and Santina with varying defense responses, assessing plant growth, physiological variables (water potential, gas exchange, and plant hydraulic conductance), and the levels of abscisic acid (ABA) and salicylic acid (SA) under two summer irrigation levels. Pss inoculation elicited a more pronounced response in ‘Santina’ compared to ‘Bing’ at 14 days post-inoculation (dpi), and those plants inoculated with Pss exhibited a slower leaf growth and reduced transpiration compared to control plants during 60 dpi. During differential irrigations, leaf area was reduced 14% and 44% in Pss inoculated plants of ‘Bing’ and ‘Santina’ respectively, under well-watered (WW) conditions, without changes in plant water status or gas exchange. Conversely, water-deficit (WD) conditions led to gas exchange limitations and a 43% decrease in plant biomass compared to that under WW conditions, with no differences between inoculation treatments. ABA levels were lower under WW than under WD at 90 dpi, while SA levels were significantly higher in Pss-inoculated plants under WW conditions. These findings underscore the influence on plant growth during summer in sweet cherry cultivars that showed a differential response to Pss inoculations and how the relationship between ABA and SA changes in plant drought level responses.

Bacterial canker is an important disease of sweet cherry plants mainly caused by Pseudomonas syringae pv. syringae (Pss). Water deficit profoundly impairs the yield of this crop. Nitric oxide (NO) is a molecule that plays an important role in the plant defense mechanisms. To evaluate the protection exerted by NO against Pss infection under normal or water-restricted conditions, sodium nitroprusside (SNP), a NO donor, was applied to sweet cherry plants cv. Lapins, before they were exposed to Pss infection under normal or water-restricted conditions throughout two seasons. Well-watered plants treated with exogenous NO presented a lower susceptibility to Pss. A lower susceptibility to Pss was also induced in plants by water stress and this effect was increased when water stress was accompanied by exogenous NO. The lower susceptibility to Pss induced either by exogenous NO or water stress was accompanied by a decrease in the internal bacterial population. In well-watered plants, exogenous NO increased the stomatal conductance and the net CO₂ assimilation. In water-stressed plants, NO induced an increase in the leaf membranes stability and proline content, but not an increase in the CO₂ assimilation or the stomatal conductance.

Pseudomonas syringae pv. syringae (Pss) is an economically significant bacterial pathogen that causes canker in sweet cherry trees. In Chile, sweet cherry (Prunus avium L.) is a key crop whose exponential production growth has increased phytosanitary pressure. However, the genetic diversity and adaptive mechanisms of local Pss populations have remained poorly understood. This study characterized 41 Pss isolates from major Chilean production regions. Their genomes were sequenced and compared with 152 public genomes from the PG2 phylogenetic group. The analysis revealed a predominance of the PG2d subgroup among the Chilean isolates, with a population structure defined by at least 18 genomic clusters, some of which are exclusive to Chile. A characteristic feature of this entire PG2d subgroup is the presence of indole-3-acetic acid (IAA) synthesis genes (iaaM and iaaH). Furthermore, this subgroup displayed a marked increase in ancestral gene gain and loss events, indicating extensive remodeling of the shell genome and supporting a model of lineage-specific adaptive evolution. We also identified lineage-specific orthogroups, structural variants of the T-PAI pathogenicity island, and a differential distribution of Hop-type effector proteins. Furthermore, an extended copper resistance operon (cop and cus systems) was detected in a subset of strains, and a dominant lineage was found to have a dual i1-type of T6SS system. These findings highlight the local diversification of Pss in Chile, likely driven by agro-environmental pressures. This study provides crucial insights into the evolution, adaptation, and pathogenic potential of this important pathogen in a crop of high strategic value.

Pattern-triggered immunity (PTI) is generally considered a conserved defense layer, but how different pattern-recognition receptors (PRRs) shape immune specificity in woody perennials remains poorly resolved. We investigated whether the bacterial MAMP flg22 and the fungal elicitor xyn11/EIX trigger generic or specialized PTI states in sweet cherry (Prunus avium). We identified and functionally characterized PaFLS2 as a plasma membrane-localized, flg22-responsive receptor-like kinase, and compared its structural architecture with the previously characterized xyn11/EIX receptor PaEIX2. Residue-interaction profiling revealed a conserved FLS2 architecture and greater modular plasticity in EIX2-like receptors. Both elicitors activated PTI-associated responses, but generated distinct resistance outcomes: flg22 preferentially restricted Pseudomonas syringae pv. syringae, whereas xyn11/EIX enhanced resistance to Botrytis cinerea and produced broader defense-associated reprogramming. Integration of gene expression, orthology-informed regulatory networks, phytohormone profiling and multivariate analyses showed that flg22 and xyn11/EIX establish partially overlapping yet discrete immune configurations. These findings support a model in which PRR identity does not merely activate PTI but biases sweet cherry immunity toward distinct hormone-associated regulatory states that shape defense specificity.