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American Society for Microbiology, Applied and Environmental Microbiology, 10(80), p. 3173-3180, 2014

DOI: 10.1128/aem.00345-14

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Xanthomonas perforans Colonization Influences Salmonella enterica in the Tomato Phyllosphere

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

ABSTRACT Salmonella enterica rarely grows on healthy, undamaged plants, but its persistence is influenced by bacterial plant pathogens. The interactions between S. enterica , Xanthomonas perforans (a tomato bacterial spot pathogen), and tomato were characterized. We observed that virulent X. perforans , which establishes disease by suppressing pathogen-associated molecular pattern (PAMP)-triggered immunity that leads to effector-triggered susceptibility, created a conducive environment for persistence of S. enterica in the tomato phyllosphere, while activation of effector-triggered immunity by avirulent X. perforans resulted in a dramatic reduction in S. enterica populations. S. enterica populations persisted at ∼10 times higher levels in leaves coinoculated with virulent X. perforans than in those where S. enterica was applied alone. In contrast, S. enterica populations were ∼5 times smaller in leaves coinoculated with avirulent X. perforans than in leaves inoculated with S. enterica alone. Coinoculation with virulent X. perforans increased S. enterica aggregate formation; however, S. enterica was not found in mixed aggregates with X. perforans . Increased aggregate formation by S. enterica may serve as the mechanism of persistence on leaves cocolonized by virulent X. perforans . S. enterica association with stomata was altered by X. perforans ; however, it did not result in appreciable populations of S. enterica in the apoplast even in the presence of large virulent X. perforans populations. Gene-for-gene resistance against X. perforans successively restricted S. enterica populations. Given the effect of this interaction, breeding for disease-resistant cultivars may be an effective strategy to limit both plant disease and S. enterica populations and, consequently, human illness.