Oxathiapiprolin, a Novel Chemical Inducer Activates the Plant Disease Resistance

Oxathiapiprolin was developed as a specific plant pathogenic oomycete inhibitor, previously shown to have highly curative and protective activities against the pepper Phytophthora blight disease under field and greenhouse tests. Therefore, it was hypothesized that oxathiapiprolin might potentially activate the plant disease resistance against pathogen infections. This study investigated the potential and related mechanism of oxathiapiprolin to activate the plant disease resistance using the bacterium Pseudomonas syringae pv tomato (Pst) and plant Arabidopsis interaction as the targeted system. Our results showed that oxathiapiprolin could activate the plant disease resistance against Pst DC3000, a non-target pathogen of oxathiapiprolin, in Arabidopsis, tobacco, and tomato plants. Our results also showed the enhanced callose deposition and H2O2 accumulation in the oxathiapiprolin-treated Arabidopsis under the induction of flg22 as the pathogen-associated molecular pattern (PAMP) treatment. Furthermore, increased levels of free salicylic acid (SA) and jasmonic acid (JA) were detected in the oxathiapiprolin-treated Arabidopsis plants compared to the mock-treated ones under the challenge of Pst DC3000. Besides, the gene expression results confirmed that at 24 h after the infiltration with Pst DC3000, the oxathiapiprolin-treated Arabidopsis plants had upregulated expression levels of the respiratory burst oxidase homolog D (RBOHD), JA-responsive gene (PDF1.2), and SA-responsive genes (PR1, PR2, and PR5) compared to the control. Taken together, oxathiapiprolin is identified as a novel chemical inducer which activates the plant disease resistance against Pst DC3000 by enhancing the callose deposition, H2O2 accumulation, and hormone SA and JA production.

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The role of water stress in plant disease resistance and the impact of water stress on the global transcriptome and survival mechanisms of the phytopathogen Pseudomonas syringae

10.31274/etd-180810-2333 ◽

2009 ◽

Author(s):

Brian Carl Freeman

Keyword(s):

Disease Resistance ◽

Water Stress ◽

Pseudomonas Syringae ◽

Plant Disease Resistance ◽

Plant Disease ◽

Global Transcriptome ◽

The Impact ◽

Survival Mechanisms

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CAMTA3 negatively regulates disease resistance through modulating immune response and extensive transcriptional reprogramming in cassava

Tree Physiology ◽

10.1093/treephys/tpaa093 ◽

2020 ◽

Vol 40 (11) ◽

pp. 1520-1533

Author(s):

Yanli Chang ◽

Yujing Bai ◽

Yunxie Wei ◽

Haitao Shi

Keyword(s):

Disease Resistance ◽

Plant Disease Resistance ◽

Transcriptional Repression ◽

Plant Disease ◽

Callose Deposition ◽

Cassava Bacterial Blight ◽

Calmodulin Binding ◽

Transcriptional Reprogramming ◽

Transcription Activators ◽

The One

Abstract As one of the important crops in the world, cassava production is seriously threatened by Xanthomonas axonopodis pv. manihotis (Xam) all year round. Calmodulin-binding transcription activators (CAMTAs) play key roles in biotic stress and abiotic stress in plants, however, their roles in cassava remain elusive. In this study, six MeCAMTAs were identified, and MeCAMTA3 with the highest induction upon Xam infection was confirmed as a transcription factor that binds to the vCGCGb motif. MeCAMTA3 negatively regulates plant disease resistance against Xam. On the one hand, MeCAMTA3 negatively regulated endogenous salicylic acid and reactive oxygen species accumulation, pathogenesis-related genes MePRs’ transcripts and callose deposition during cassava-Xam interaction but not under control conditions. On the other hand, RNA sequencing showed extensive transcriptional reprogramming by MeCAMTA3, especially 18 genes with a vCGCGb motif in the promoter region in hormone signaling, antioxidant signaling and other disease resistance signaling. Notably, chromatin immunoprecipitation-polymerase chain reaction showed that eight of these genes might be directly regulated by MeCAMTA3 through transcriptional repression. In summary, MeCAMTA3 negatively regulates plant disease resistance against cassava bacterial blight through modulation of multiple immune responses during cassava-Xam interaction and extensive transcriptional reprogramming.

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Suppressors of the Arabidopsis lsd5 Cell Death Mutation Identify Genes Involved in Regulating Disease Resistance Responses

Genetics ◽

10.1093/genetics/151.1.305 ◽

1999 ◽

Vol 151 (1) ◽

pp. 305-319

Author(s):

Jean-Benoit Morel ◽

Jeffery L Dangl

Keyword(s):

Cell Death ◽

Disease Resistance ◽

Pseudomonas Syringae ◽

Plant Disease Resistance ◽

Plant Disease ◽

Disease Susceptibility ◽

Bacterial Pathogen ◽

Hypersensitive Reaction ◽

Cell Death Phenotype ◽

New Mutations

Abstract Cell death is associated with the development of the plant disease resistance hypersensitive reaction (HR). Arabidopsis lsd mutants that spontaneously exhibit cell death reminiscent of the HR were identified previously. To study further the regulatory context in which cell death acts during disease resistance, one of these mutants, lsd5, was used to isolate new mutations that suppress its cell death phenotype. Using a simple lethal screen, nine lsd5 cell death suppressors, designated phx (for the mythological bird Phoenix that rises from its ashes), were isolated. These mutants were characterized with respect to their response to a bacterial pathogen and oomycete parasite. The strongest suppressors—phx2, 3, 6, and 11-1—showed complex, differential patterns of disease resistance modifications. These suppressors attenuated disease resistance to avirulent isolates of the biotrophic Peronospora parasitica pathogen, but only phx2 and phx3 altered disease resistance to avirulent strains of Pseudomonas syringae pv tomato. Therefore, some of these phx mutants define common regulators of cell death and disease resistance. In addition, phx2 and phx3 exhibited enhanced disease susceptibility to different virulent pathogens, confirming probable links between the disease resistance and susceptibility pathways.

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Faculty Opinions recommendation of High throughput virus-induced gene silencing implicates heat shock protein 90 in plant disease resistance.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1003609.201391 ◽

2003 ◽

Author(s):

Jen Sheen

Keyword(s):

Disease Resistance ◽

Heat Shock ◽

Heat Shock Protein ◽

Gene Silencing ◽

High Throughput ◽

Plant Disease Resistance ◽

Plant Disease ◽

Heat Shock Protein 90 ◽

Virus Induced Gene Silencing

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Faculty Opinions recommendation of A gain-of-function mutation in a plant disease resistance gene leads to constitutive activation of downstream signal transduction pathways in suppressor of npr1-1, constitutive 1.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1016258.200354 ◽

2003 ◽

Author(s):

Laurence Rahme

Keyword(s):

Signal Transduction ◽

Disease Resistance ◽

Resistance Gene ◽

Plant Disease Resistance ◽

Plant Disease ◽

Signal Transduction Pathways ◽

Disease Resistance Gene ◽

Gain Of Function ◽

Constitutive Activation ◽

Plant Disease Resistance Gene

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Transcriptomic Analyses on the Role of Nitric Oxide in Plant Disease Resistance

Current Issues in Molecular Biology ◽

10.21775/9781910190357.11 ◽

2016 ◽

Keyword(s):

Nitric Oxide ◽

Disease Resistance ◽

Plant Disease Resistance ◽

Plant Disease

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The Leucine-Rich Repeat Domain Can Determine Effective Interaction Between RPS2 and Other Host Factors in Arabidopsis RPS2-Mediated Disease Resistance

Genetics ◽

10.1093/genetics/158.1.439 ◽

2001 ◽

Vol 158 (1) ◽

pp. 439-450 ◽

Cited By ~ 4

Author(s):

Diya Banerjee ◽

Xiaochun Zhang ◽

Andrew F Bent

Keyword(s):

Disease Resistance ◽

Pseudomonas Syringae ◽

Plant Disease Resistance ◽

Effective Interaction ◽

Molecular Genetic ◽

Defense Responses ◽

Host Factors ◽

Leucine Rich Repeat ◽

Domain Swap ◽

Allele Specific

Abstract Like many other plant disease resistance genes, Arabidopsis thaliana RPS2 encodes a product with nucleotide-binding site (NBS) and leucine-rich repeat (LRR) domains. This study explored the hypothesized interaction of RPS2 with other host factors that may be required for perception of Pseudomonas syringae pathogens that express avrRpt2 and/or for the subsequent induction of plant defense responses. Crosses between Arabidopsis ecotypes Col-0 (resistant) and Po-1 (susceptible) revealed segregation of more than one gene that controls resistance to P. syringae that express avrRpt2. Many F2 and F3 progeny exhibited intermediate resistance phenotypes. In addition to RPS2, at least one additional genetic interval associated with this defense response was identified and mapped using quantitative genetic methods. Further genetic and molecular genetic complementation experiments with cloned RPS2 alleles revealed that the Po-1 allele of RPS2 can function in a Col-0 genetic background, but not in a Po-1 background. The other resistance-determining genes of Po-1 can function, however, as they successfully conferred resistance in combination with the Col-0 allele of RPS2. Domain-swap experiments revealed that in RPS2, a polymorphism at six amino acids in the LRR region is responsible for this allele-specific ability to function with other host factors.

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