The metabolic transition during disease following infection of Arabidopsis thaliana by Pseudomonas syringae pv. tomato

The auxin indole-3-acetic acid (IAA) is a plant hormone that not only regulates plant growth and development but also plays important roles in plant-microbe interactions. We previously reported that IAA alters expression of several virulence-related genes in the plant pathogen Pseudomonas syringae pv. tomato strain DC3000 ( Pto DC3000). To learn more about the impact of IAA on regulation of Pto DC3000 gene expression we performed a global transcriptomic analysis of bacteria grown in culture, in the presence or absence of exogenous IAA. We observed that IAA repressed expression of genes involved in the Type III secretion (T3S) system and motility and promoted expression of several known and putative transcriptional regulators. Several of these regulators are orthologs of factors known to regulate stress responses and accordingly expression of several stress response-related genes was also upregulated by IAA. Similar trends in expression for several genes were also observed by RT-qPCR. Using an Arabidopsis thaliana auxin receptor mutant that accumulates elevated auxin, we found that many of the P. syringae genes regulated by IAA in vitro were also regulated by auxin in planta . Collectively the data indicate that IAA modulates many aspects of Pto DC3000 biology, presumably to promote both virulence and survival under stressful conditions, including those encountered in or on plant leaves. IMPORTANCE Indole-3-acetic acid (IAA), a form of the plant hormone auxin, is used by many plant-associated bacteria as a cue to sense the plant environment. Previously, we showed that IAA can promote disease in interactions between the plant pathogen Pseudomonas syringae strain Pto DC000 and one of its hosts, Arabidopsis thaliana . However, the mechanisms by which IAA impacts the biology of Pto DC3000 and promotes disease are not well understood. Here we demonstrate that IAA is a signal molecule that regulates gene expression in Pto DC3000. The presence of exogenous IAA affects expression of over 700 genes in the bacteria, including genes involved in Type III secretion and genes involved in stress response. This work offers insight into the roles of auxin promoting pathogenesis.

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Inositol hexa kis phosphate biosynthesis underpins PAMP‐triggered immunity to Pseudomonas syringae pv. tomato in Arabidopsis thaliana but is dispensable for establishment of systemic acquired resistance

Molecular Plant Pathology ◽

10.1111/mpp.12902 ◽

2019 ◽

Vol 21 (3) ◽

pp. 376-387

Author(s):

Jacquelyne S. Y. Poon ◽

Ruth E. Le Fevre ◽

John P. Carr ◽

David E. Hanke ◽

Alex M. Murphy

Keyword(s):

Arabidopsis Thaliana ◽

Pseudomonas Syringae ◽

Systemic Acquired Resistance ◽

Acquired Resistance

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Progesterone moderates damage in Arabidopsis thaliana caused by infection with Pseudomonas syringae or P. fluorescens

Biologia Plantarum ◽

10.1007/s10535-012-0142-y ◽

2013 ◽

Vol 57 (1) ◽

pp. 169-173 ◽

Cited By ~ 7

Author(s):

A. Janeczko ◽

I. Tobias ◽

A. Skoczowski ◽

F. Dubert ◽

G. Gullner ◽

...

Keyword(s):

Arabidopsis Thaliana ◽

Pseudomonas Syringae

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Bacillus cereus AR156 Activates Defense Responses to Pseudomonas syringae pv. tomato in Arabidopsis thaliana Similarly to flg22

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi-10-17-0240-r ◽

2018 ◽

Vol 31 (3) ◽

pp. 311-322 ◽

Cited By ~ 9

Author(s):

Shune Wang ◽

Ying Zheng ◽

Chun Gu ◽

Chan He ◽

Mengying Yang ◽

...

Keyword(s):

Arabidopsis Thaliana ◽

Bacillus Cereus ◽

Pseudomonas Syringae ◽

Transcriptional Profiling ◽

Quantitative Polymerase Chain Reaction ◽

Polymerase Chain Reaction Analysis ◽

Defense Responses ◽

Systemic Resistance ◽

Callose Deposition ◽

Plant Growth Promoting

Bacillus cereus AR156 (AR156) is a plant growth–promoting rhizobacterium capable of inducing systemic resistance to Pseudomonas syringae pv. tomato in Arabidopsis thaliana. Here, we show that, when applied to Arabidopsis leaves, AR156 acted similarly to flg22, a typical pathogen-associated molecular pattern (PAMP), in initiating PAMP-triggered immunity (PTI). AR156-elicited PTI responses included phosphorylation of MPK3 and MPK6, induction of the expression of defense-related genes PR1, FRK1, WRKY22, and WRKY29, production of reactive oxygen species, and callose deposition. Pretreatment with AR156 still significantly reduced P. syringae pv. tomato multiplication and disease severity in NahG transgenic plants and mutants sid2-2, jar1, etr1, ein2, npr1, and fls2. This suggests that AR156-induced PTI responses require neither salicylic acid, jasmonic acid, and ethylene signaling nor flagella receptor kinase FLS2, the receptor of flg22. On the other hand, AR156 and flg22 acted in concert to differentially regulate a number of AGO1-bound microRNAs that function to mediate PTI. A full-genome transcriptional profiling analysis indicated that AR156 and flg22 activated similar transcriptional programs, coregulating the expression of 117 genes; their concerted regulation of 16 genes was confirmed by real-time quantitative polymerase chain reaction analysis. These results suggest that AR156 activates basal defense responses to P. syringae pv. tomato in Arabidopsis, similarly to flg22.

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Transcript and metabolite analysis of the Trichoderma-induced systemic resistance response to Pseudomonas syringae in Arabidopsis thaliana

Microbiology ◽

10.1099/mic.0.052621-0 ◽

2012 ◽

Vol 158 (1) ◽

pp. 139-146 ◽

Cited By ~ 102

Author(s):

Yariv Brotman ◽

Jan Lisec ◽

Michaël Méret ◽

Ilan Chet ◽

Lothar Willmitzer ◽

...

Keyword(s):

Arabidopsis Thaliana ◽

Pseudomonas Syringae ◽

Induced Systemic Resistance ◽

Systemic Resistance ◽

Metabolite Analysis ◽

Resistance Response

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Induced Systemic Resistance in Arabidopsis thaliana Against Pseudomonas syringae pv. tomato by 2,4-Diacetylphloroglucinol-Producing Pseudomonas fluorescens

Phytopathology ◽

10.1094/phyto-08-11-0222 ◽

2012 ◽

Vol 102 (4) ◽

pp. 403-412 ◽

Cited By ~ 89

Author(s):

David M. Weller ◽

Dmitri V. Mavrodi ◽

Johan A. van Pelt ◽

Corné M. J. Pieterse ◽

Leendert C. van Loon ◽

...

Keyword(s):

Arabidopsis Thaliana ◽

Pseudomonas Fluorescens ◽

Induced Resistance ◽

Pseudomonas Syringae ◽

Induced Systemic Resistance ◽

Signal Transduction Pathway ◽

Systemic Resistance ◽

Wild Type ◽

Challenge Inoculation ◽

Dependent Signal

Pseudomonas fluorescens strains that produce the polyketide antibiotic 2,4-diacetylphloroglucinol (2,4-DAPG) are among the most effective rhizobacteria that suppress root and crown rots, wilts, and damping-off diseases of a variety of crops, and they play a key role in the natural suppressiveness of some soils to certain soilborne pathogens. Root colonization by 2,4-DAPG-producing P. fluorescens strains Pf-5 (genotype A), Q2-87 (genotype B), Q8r1-96 (genotype D), and HT5-1 (genotype N) produced induced systemic resistance (ISR) in Arabidopsis thaliana accession Col-0 against bacterial speck caused by P. syringae pv. tomato. The ISR-eliciting activity of the four bacterial genotypes was similar, and all genotypes were equivalent in activity to the well-characterized strain P. fluorescens WCS417r. The 2,4-DAPG biosynthetic locus consists of the genes phlHGF and phlACBDE. phlD or phlBC mutants of Q2-87 (2,4-DAPG minus) were significantly reduced in ISR activity, and genetic complementation of the mutants restored ISR activity back to wild-type levels. A phlF regulatory mutant (overproducer of 2,4-DAPG) had ISR activity equivalent to the wild-type Q2-87. Introduction of DAPG into soil at concentrations of 10 to 250 μM 4 days before challenge inoculation induced resistance equivalent to or better than the bacteria. Strain Q2-87 induced resistance on transgenic NahG plants but not on npr1-1, jar1, and etr1 Arabidopsis mutants. These results indicate that the antibiotic 2,4-DAPG is a major determinant of ISR in 2,4-DAPG-producing P. fluorescens, that the genotype of the strain does not affect its ISR activity, and that the activity induced by these bacteria operates through the ethylene- and jasmonic acid-dependent signal transduction pathway.

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