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Infect Immun. 2005 Jan;73(1):464-75.

Enterococcus faecalis mammalian virulence-related factors exhibit potent pathogenicity in the Arabidopsis thaliana plant model.

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  • 1Department of Horticulture and Landscape Architecture, Colorado State University, 217 Shepardson Building, Fort Collins, CO 80523-1173, USA.


Some pathogenic bacteria belong to a large, diverse group of species capable of infecting plants, animals, and humans. Enterococcus faecalis is an opportunistic human pathogen capable of infecting patients with a deficient immune system. Here we report that three E. faecalis strains (FA-2-2, V583, and OG1RF) are capable of infecting the leaves and roots of the model plant species Arabidopsis thaliana, causing plant mortality 7 days postinoculation. We found that E. faecalis pathogenesis in A. thaliana leaves is determined by the following series of events: attachment to leaf surface, entry through stomata or wounds, and colonization in intercellular spaces, leading to rotting and to the disruption of plant cell wall and membrane structures. The three E. faecalis strains colonize the roots of A. thaliana by forming a mosaic of large clusters of live bacteria on the root surface, as observed by scanning electron microscopy, phase-contrast microscopy, and fluorescence microscopy. To dissect the involvement of mammalian virulence-related factors in plant pathogenicity, we tested E. faecalis mutant strains DeltafsrA (TX5240), DeltafsrB (TX5266), DeltafsrC (TX5242), DeltagelE (TX5264), and DeltasprE (TX5243), which correspond to virulence factors involved in pathogenesis in different animal models. Two E. faecalis virulence-related factors that play an important role in mammalian and nematode models of infection, a putative quorum-sensing system (DeltafsrB) and serine protease (DeltasprE), were also found to be important for plant pathogenesis. The development of an E. faecalis-A. thaliana model system could potentially be used to circumvent certain inherent limitations that an animal model imposes on the identification and study of virulence factors. Furthermore, our study suggests an evolutionary crossover of virulence factors in plant, animal, and nematode pathogenesis.

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