Enterococcus faecalis mammalian virulence-related factors exhibit potent pathogenicity in the Arabidopsis thaliana
Ajay K Jha1, Harsh P Bais, Jorge M Vivanco
1Department of Horticulture and Landscape Architecture, Colorado State University, 217 Shepardson Building, Fort Collins, CO 80523-1173, USA.
Abstract:
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.
Insights
Enterococcus faecalis, an opportunistic pathogen, infects the model plant Arabidopsis thaliana, causing mortality. Key virulence factors like quorum-sensing and serine protease are crucial for plant pathogenesis, suggesting evolutionary crossover.
Area of Science:
- Microbiology
- Plant Pathology
- Bacterial Pathogenesis
Background:
- Pathogenic bacteria can infect diverse hosts, including plants, animals, and humans.
- Enterococcus faecalis is an opportunistic pathogen affecting immunocompromised individuals.
- The plant model Arabidopsis thaliana is susceptible to E. faecalis infection.
Purpose of the Study:
- To investigate the pathogenicity of Enterococcus faecalis in Arabidopsis thaliana.
- To identify bacterial virulence factors involved in plant infection.
- To explore the potential of an E. faecalis-A. thaliana model for studying virulence factors.
Main Methods:
- Inoculation of Arabidopsis thaliana leaves and roots with three E. faecalis strains.
- Microscopic analysis (SEM, phase-contrast, fluorescence) to observe bacterial colonization.
- Testing of E. faecalis mutant strains lacking specific virulence factors (DeltafsrA, DeltafsrB, DeltafsrC, DeltagelE, DeltasprE).
Main Results:
- E. faecalis successfully infected A. thaliana leaves and roots, causing plant mortality within 7 days.
- Bacterial pathogenesis involved attachment, entry via stomata/wounds, and intercellular colonization, leading to tissue damage.
- Virulence factors such as the quorum-sensing system (DeltafsrB) and serine protease (DeltasprE) were critical for plant pathogenesis.
Conclusions:
- Enterococcus faecalis can infect and cause mortality in Arabidopsis thaliana.
- Specific mammalian virulence factors are conserved and play a role in plant pathogenesis.
- The E. faecalis-A. thaliana model offers a valuable system for studying bacterial virulence factors and suggests evolutionary links in pathogenesis across kingdoms.
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