Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanisms controlling plant resistance to necrotrophic fungal pathogens are poorly understood. We previously reported on Ep5C, a gene shown to be induced by the H(2)O(2) generated during a plant-pathogen interaction. To identify novel plant components operating in pathogen-induced signaling cascades, we initiated a large-scale screen using Arabidopsis thaliana plants carrying the beta-glucuronidase reporter gene under control of the H(2)O(2)-responsive Ep5C promoter. Here, we report the identification and characterization of a mutant, ocp3 (for overexpressor of cationic peroxidase 3), in which the reporter construct is constitutively expressed. Healthy ocp3 plants show increased accumulation of H(2)O(2) and express constitutively the Glutathione S-transferase1 and Plant Defensine 1.2 marker genes, but not the salicylic acid (SA)-dependent pathogenesis-related PR-1 gene. Strikingly, the ocp3 mutant shows enhanced resistance to the necrotrophic pathogens Botrytis cinerea and Plectosphaerella cucumerina. Conversely, resistance to virulent forms of the biotrophic oomycete Hyaloperonospora parasitica and the bacterial pathogen Pseudomonas syringae pv tomato DC3000 remains unaffected in ocp3 plants when compared with wild-type plants. Consistently with this, ocp3 plants are not affected in SA perception and express normal levels of PR genes after pathogen attack. To analyze signal transduction pathways where ocp3 operates, epistasis analyses between ocp3 and pad4, nahG, npr1, ein2, jin1, or coi1 were performed. These studies revealed that the resistance signaling to necrotrophic infection in ocp3 is fully dependent on appropriate perception of jasmonic acid through COI1 and does not require SA or ethylene perception through NPR1 or EIN2, respectively. The OCP3 gene encodes a homeodomain transcription factor that is constitutively expressed in healthy plants but repressed in response to infection by necrotrophic fungi. Together, these results suggest that OCP3 is an important factor for the COI1-dependent resistance of plants to infection by necrotrophic pathogens.
 ...
PMID:An Arabidopsis homeodomain transcription factor, OVEREXPRESSOR OF CATIONIC PEROXIDASE 3, mediates resistance to infection by necrotrophic pathogens. 1592 48

Salicylic acid (SA) has been proposed to antagonize jasmonic acid (JA) biosynthesis and signaling. We report, however, that in salicylate hydroxylase-expressing tobacco (Nicotiana tabacum) plants, where SA levels were reduced, JA levels were not elevated during a hypersensitive response elicited by Pseudomonas syringae pv phaseolicola. The effects of cotreatment with various concentrations of SA and JA were assessed in tobacco and Arabidopsis (Arabidopsis thaliana). These suggested that there was a transient synergistic enhancement in the expression of genes associated with either JA (PDF1.2 [defensin] and Thi1.2 [thionin]) or SA (PR1 [PR1a-beta-glucuronidase in tobacco]) signaling when both signals were applied at low (typically 10-100 microm) concentrations. Antagonism was observed at more prolonged treatment times or at higher concentrations. Similar results were also observed when adding the JA precursor, alpha-linolenic acid with SA. Synergic effects on gene expression and plant stress were NPR1- and COI1-dependent, SA- and JA-signaling components, respectively. Electrolyte leakage and Evans blue staining indicated that application of higher concentrations of SA + JA induced plant stress or death and elicited the generation of apoplastic reactive oxygen species. This was indicated by enhancement of hydrogen peroxide-responsive AoPR10-beta-glucuronidase expression, suppression of plant stress/death using catalase, and direct hydrogen peroxide measurements. Our data suggests that the outcomes of JA-SA interactions could be tailored to pathogen/pest attack by the relative concentration of each hormone.
 ...
PMID:The outcomes of concentration-specific interactions between salicylate and jasmonate signaling include synergy, antagonism, and oxidative stress leading to cell death. 1637 44

SNC1 (suppressor of NPR1, constitutive 1) is a haplotype-specific Toll and interleukin-1 receptor-like nucleotide-binding site leucine-rich repeat type of resistance (R)-like gene possibly mediating race-specific disease resistance. Inactivation of its negative regulator BON1 (BONZAI1)/CPN1 and BAP1 genes or upregulation of its expression epigenetically lead to constitutive defense responses and dwarf phenotype. Here, we report an autoactivation of SNC1 by introducing it into Arabidopsis as a transgene. The SNC1 genomic fragment confers a dwarf phenotype induced by defense response upregulation associated with a higher SNC1 transcript level. Analysis of the beta-glucuronidase reporter gene under the control of the SNC1 promoter suggests three modes of regulation on the SNC1 transcript level: a repression by the chromosomal structure, a feedback amplification from SNC1 on its promoter sequences, and a repression by BON1. These regulations appear to be independent of each other. The regulation of SNC1 possibly exemplifies a universally complex control of R genes to ensure a repression of R activation under nonstress conditions and a robust activation of defense responses once the R gene is induced.
 ...
PMID:The TIR-NB-LRR gene SNC1 is regulated at the transcript level by multiple factors. 1797 56

TGA factors play a key role in plant defense by binding to the promoter region of defense genes, inducing expression. Salicylic acid (SA) induces the expression of the gene encoding NIMIN-1, which interacts with NPR1/NIM1, a key regulator of systemic acquired resistance. We investigated whether the TGA2-binding motif TGACG located upstream of the NIMIN-1 gene is necessary for SA induction of NIMIN-1 expression. A mutated version of the NIMIN-1 promoter was created by site-directed mutagenesis. We generated T-DNA constructs in which native NIMIN-1 and mutated promoters were fused to green fluorescent protein and beta-glucuronidase reporters. We produced transgenic Arabidopsis plants and observed NIMIN-1 promoter-driven green fluorescent protein expression in the roots, petiole and leaves. Constructs were agroinfiltrated into the leaves for transient quantitative assays of gene expression. Using quantitative real-time RT-PCR, we characterized the normal gene response to SA and compared it to the response of the mutant version of the NIMIN-1 promoter. Both the native NIMIN-1 construct and an endogenous copy of NIMIN-1 were induced by SA. However, the mutated promoter construct was much less sensitive to SA than the native NIMIN-1 promoter, indicating that this TGA2-binding motif is directly involved in the modulation of SA-induced NIMIN-1 expression in Arabidopsis.
 ...
PMID:Functional analysis of a TGA factor-binding site located in the promoter region controlling salicylic acid-induced NIMIN-1 expression in Arabidopsis. 2019 73