Variability in the resistance to bacterial spot causal agents Xanthomonas euvesicatoria P and Xanthomonas vesicatoria PT2 among Bulgarian and introduced pepper varieties

Abstract. Bacterial spot in pepper (Capsicum annuum L.) is caused by Xanthomonas euvesicatoria and X. vesicatoria. The natural Bulgarian population of X. vesicatoria belongs to pepper-tomato pathotypes (PT), whereas Macedonian population of X. euvesicatoria refers to pepper pathotypes (P). Bacterial spot of pepper caused by X. vesicatoria and X. euvesicatoria has become a very serious disease in Bulgaria during the past few years. The use of resistant pepper cultivars is the most economically and technically efficient method for control. Pepper varieties with immune and/or resistant reaction were not found in this study. Moderately susceptible to both pathogens were the following varieties: Kapia UV-Vertus, Sofijska kapia and Familiya of Kapia type, Quadrato D"Asti Giallo of Dolma type and Chorbadzhiyski of long pungent fruits. All varieties with cone-shaped fruits and the ones for sweet powder performed with highly susceptible reaction to X. еuvesicatoria

The emerging case for epigenetic regulation of plant immunity

In order to cause a disease, pathogens need to break the plant cell wall and to this purpose they secrete degrading enzymes towards various cell wall components. Several oligosaccharides released during pathogenesis, such as the Oligogalacturonides (OGs) and Cellodextrins (CDs) upon the breakdown of the homogalacturonan and cellulose respectively, act as Damage-Associated Molecular Patterns (DAMPs) and activate immunity. However, an over-accumulation of DAMPs may lead to a hyper-immunity characterized by a reduction of growth and, sometimes, cell death; for example, an over-accumulation of OGs leads to a hyper-immunity phenotype. Therefore, it is conceivable that the response to DAMPs must be controlled through homeostatic mechanisms to prevent hyper-immunity. We have discovered that four Arabidopsis Berberine Bridge Enzyme-like (BBE-like) proteins (OGOX1-4) oxidize OGs and impair their elicitor activity. We have also discovered another member of the BBE-like enzymes (CELLOX) which is expressed coordinately with OGOX1 during immunity and that specifically oxidizes CDs, also impairing their elicitor activity. Moreover, plants overexpressing OGOX1 or CELLOX display an enhanced resistance to Botrytis cinerea, likely because oxidized OGs and CDs are a less valuable carbon source for Botrytis. Thus, the capacity of impairing the activity of the cell wall-derived DAMPs is one important feature of BBE-like proteins that it may serve for the homeostatic control of the level of DAMPs

Repeated gain and loss of a single gene modulates the evolution of vascular plant pathogen lifestyles

International audienceVascular plant pathogens travel long distances through host veins, leading to life-threatening, systemic infections. In contrast, nonvascular pathogens remain restricted to infection sites, triggering localized symptom development. The contrasting features of vascular and nonvascular diseases suggest distinct etiologies, but the basis for each remains unclear. Here, we show that the hydrolase CbsA acts as a phenotypic switch between vascular and nonvascular plant pathogenesis. cbsA was enriched in genomes of vascular phytopathogenic bacteria in the family Xanthomonadaceae and absent in most nonvascular species. CbsA expression allowed nonvascular Xanthomonas to cause vascular blight, while cbsA mutagenesis resulted in reduction of vascular or enhanced nonvascular symptom development. Phylogenetic hypothesis testing further revealed that cbsA was lost in multiple nonvascular lineages and more recently gained by some vascular subgroups, suggesting that vascular pathogenesis is ancestral. Our results overall demonstrate how the gain and loss of single loci can facilitate the evolution of complex ecological traits

Repeated gain and loss of a single gene modulates the evolution of vascular plant pathogen lifestyles

Vascular plant pathogens travel long distances through host veins, leading to life-threatening, systemic infections. In contrast, nonvascular pathogens remain restricted to infection sites, triggering localized symptom development. The contrasting features of vascular and nonvascular diseases suggest distinct etiologies, but the basis for each remains unclear. Here, we show that the hydrolase CbsA acts as a phenotypic switch between vascular and nonvascular plant pathogenesis. cbsA was enriched in genomes of vascular phytopathogenic bacteria in the family Xanthomonadaceae and absent in most nonvascular species. CbsA expression allowed nonvascular Xanthomonas to cause vascular blight, while cbsA mutagenesis resulted in reduction of vascular or enhanced nonvascular symptom development. Phylogenetic hypothesis testing further revealed that cbsA was lost in multiple nonvascular lineages and more recently gained by some vascular subgroups, suggesting that vascular pathogenesis is ancestral. Our results overall demonstrate how the gain and loss of single loci can facilitate the evolution of complex ecological traits