Abstract

BackgroundPseudomonas syringae is pathogenic to a large number of plant species. For host colonization and disease progression, strains of this bacterium utilize an array of type III-secreted effectors and other virulence factors, including small secreted molecules such as syringolin A, a peptide derivative that inhibits the eukaryotic proteasome. In strains colonizing dicotyledonous plants, the compound was demonstrated to suppress the salicylic-acid-dependent defense pathway. Here, we analyze virulence factors of three strains colonizing wheat (Triticum aestivum): P. syringae pathovar syringae (Psy) strains B64 and SM, as well as P. syringae BRIP34876. These strains have a relatively small repertoire of only seven to eleven type III secreted effectors (T3Es) and differ in their capacity to produce syringolin A. The aim of this study was to analyze the contribution of various known virulence factors in the context of a small T3E repertoire.ResultsWe demonstrate that syringolin A production enhances disease symptom development upon direct infiltration of strains into wheat leaves. However, it is not universally required for colonization, as Psy SM, which lacks syringolin biosynthesis genes, reaches cell densities comparable to syringolin A producer P. syringae BRIP34876. Next, we show that despite the small set of T3E-encoding genes, the type III secretion system remains the key pathogenicity determinant in these strains, and that phenotypic effects of deleting T3E-coding genes become apparent only when multiple effectors are removed.ConclusionsWhereas production of syringolin A is not required for successful colonization of wheat leaves by P. syringae strains, its production results in increased lesion formation. Despite the small number of known T3Es encoded by the analyzed strains, the type III secretion system is essential for endophytic growth of these strains.Electronic supplementary materialThe online version of this article (doi:10.1186/s12866-014-0304-5) contains supplementary material, which is available to authorized users.

Highlights

  • Pseudomonas syringae is pathogenic to a large number of plant species

  • Syringolin production shows strain-specific effects on symptom development in wheat In order to search for a potential role of syringolin A in the infection process on wheat, wild type pathovar syringae (Psy) SM, Psy B64, and BRIP34876 were assayed

  • Psy B64 and BRIP34876 were compared with their respective sylC knock-out mutants that are deficient in syringolin A production (Psy B64 sylC_KO and BRIP34876 sylC_KO)

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Summary

Introduction

Pseudomonas syringae is pathogenic to a large number of plant species. For host colonization and disease progression, strains of this bacterium utilize an array of type III-secreted effectors and other virulence factors, including small secreted molecules such as syringolin A, a peptide derivative that inhibits the eukaryotic proteasome. We analyze virulence factors of three strains colonizing wheat (Triticum aestivum): P. syringae pathovar syringae (Psy) strains B64 and SM, as well as P. syringae BRIP34876 These strains have a relatively small repertoire of only seven to eleven type III secreted effectors (T3Es) and differ in their capacity to produce syringolin A. The majority of characterized T3Es from P. syringae were demonstrated to be involved in the suppression of plant immune responses [16,17,18] This is achieved in a variety of ways, and several effectors were demonstrated to degrade components of a defense signaling pathway either directly [19,20] or by ubiquitylation [21]. Due to functional redundancy, strains isolated from the same host often show variability in their effector sets [28,29,30]

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