Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.25.1 (proteasome)
28,817 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We previously isolated, by differential display and 5' RACE (rapid amplification of cDNA ends), cDNAs corresponding to genes activated following cryptogein treatment of tobacco cell suspensions, among them tcI 7 (tcI for tobacco cryptogein Induced), a gene encoding a beta-subunit of proteasome. Here, we report that tcl 7 was up-regulated in tobacco plants treated with elicitins (cryptogein and parasiticein) that have been shown to induce a systemic acquired resistance (SAR). Moreover, subsequent inoculation of tobacco with the pathogen Phytophthora parasitica var. nicotianae (Ppn) was shown to induce an additional activation of tcI 7 in tobacco plants pretreated with cryptogein. We also showed an up-regulation of tcI 7 by salicylic acid (SA). Moreover, accumulation of tcI 7 transcripts after treatment with cryptogein or with SA only occurred in NahG 9-tobacco plants that do not express the salicylate hydroxylase and thus are able to accumulate SA and develop a SAR. Suppressed accumulation of tcI 7 transcripts in NahG 8+ tobacco plants after cryptogein or SA treatment correlated with the loss of SAR. H2O2 was also shown to up-regulate tcI 7 in tobacco plants. Using gene walking by PCR we cloned and sequenced the 5' flanking region of tcI 7 containing hypothetical regulatory sequences, especially myb and NF-kappaB boxes, that could be responsible for the regulation of tcI 7 by salicylic acid and H2O2 respectively.
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PMID:Induction of tcI 7, a gene encoding a beta-subunit of proteasome, in tobacco plants treated with elicitins, salicylic acid or hydrogen peroxide. 1068 30

The 26S proteasome involved in degradation of proteins covalently modified with polyubiquitin consists of the 20S proteasome and 19S regulatory complex. The NbPAF gene encoding the alpha6 subunit of the 20S proteasome was identified from Nicotiana benthamiana. NbPAF exhibits high sequence homology with the corresponding genes from Arabidopsis, human and yeast. The deduced amino acid sequence of NbPAF reveals that this protein contains the proteasome alpha-type subunits signature and nuclear localization signal at the N-terminus. The genomic Southern blot analysis suggests that the N. benthamiana genome contains one copy of NbPAF. The NbPAF mRNA was detected abundantly in flowers and weakly in roots and stems, but it was almost undetectable in mature leaves. In response to stresses, accumulation of the NbPAF mRNA was stimulated by methyl jasmonate, NaCl and salicylic acid, but not by abscisic acid and cold treatment in leaves. The NbPAF-GFP fusion protein was localized in the cytoplasm and nucleus.
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PMID:Molecular characterization of NbPAF encoding the alpha6 subunit of the 20S proteasome in Nicotiana benthamiana. 1266 72

Recent characterization of several genes involved in plant defense responses suggested that ubiquitin-mediated protein degradation has a role in these responses. We isolated two cDNAs (NtUBA1 and NtUBA2) encoding ubiquitin-activating enzyme (E1) from Nicotiana tabacum cv. BY-2. The open reading frames of both encoded 1080 amino acids, corresponding to molecular masses of 120 kDa. The E1s and corresponding transcripts were upregulated by infection with tobacco mosaic virus (TMV) and tomato mosaic virus (ToMV), and to a lesser extent by cucumber mosaic virus (CMV). Furthermore, they were also upregulated by wounding stress, and the plant hormones salicylic acid, jasmonic acid and the ethylene precursor, aminocyclopropane-1-carboxylic acid (ACC). Our findings support the idea that the ubiquitin-proteasome system plays a role in plant disease defenses.
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PMID:The tobacco ubiquitin-activating enzymes NtE1A and NtE1B are induced by tobacco mosaic virus, wounding and stress hormones. 1587 7

Many plant developmental and stress responses require the coordinated interaction of the jasmonate and other signalling pathways, such as those for ethylene, salicylic acid and abscisic acid. Recent research in Arabidopsis has uncovered several key players that regulate crosstalk between these signalling pathways and that shed light on the molecular mechanisms modulating this coordinated interaction. Genes that are involved in the regulation of protein stability through the ubiquitin-proteasome pathway (COI1, AXR1 and SGT1b), signalling proteins (MPK4) and transcription factors (AtMYC2, ERF1, NPR1 and WRKY70) form a regulatory network that allows the plant to fine-tune specific responses to different stimuli.
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PMID:Molecular players regulating the jasmonate signalling network. 1603 1

The ubiquitin-proteasome pathway is the major route for protein degradation in eukaryotes. We show here that this pathway can be inhibited in Arabidopsis thaliana by expression of a ubiquitin variant that contains Arg instead of Lys at position 48 (ubR48). A major consequence of ubR48 expression is the induction of cell death. Cell death induction coincides with the appearance of reactive oxygen intermediates, but is independent of salicylic acid. We found changes in expression of some defense-related genes, but these changes are apparently insufficient to cause alterations in the response to a bacterial pathogen. Expression of ubR48 from an inducible gene allowed investigation of kinetic parameters of cell death induction. In the absence of additional stress factors, slow death processes dominate if the transgene is induced in seedlings older than 2 weeks. The inducible gene also allowed isolation of suppressor mutants. Expression of ubR48 may cause changes similar to inhibition of the proteasome, which also induces various forms of cell death. Thus, ubR48 is a tool to manipulate protein turnover and to probe cell death programs in plants.
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PMID:Expression of the ubiquitin variant ubR48 decreases proteolytic activity in Arabidopsis and induces cell death. 1620 Apr 8

Volatile esters, primarily synthesized in peel tissues, are major aromatic components of apple fruits [Malus sylvestris (L.) Mill. var. domestica (Borkh.) Mansf.]. The use of cold storage combined with 1-methylcyclopropene (1-MCP) treatment prolongs the life of apples but represses the regeneration of esters during poststorage ripening. In this study, the regeneration of total esters was significantly increased in apple fruits treated with salicylic acid (SA) and Ethephon (ETH) that had been treated once or twice with 1-MCP. However, methyl jasmonate (MeJA) treatment resulted in regeneration of total esters after a single 1-MCP treatment. To determine the mechanism by which SA, ETH, and MeJA regulate ester regeneration, the apple alcohol acyltransferase gene (MdAAT2) was investigated at the mRNA, protein, and enzyme activity levels. Genes associated with ethylene perception were also investigated by RT-PCR. The results suggest that MdAAT2 controls ester regeneration and that MdETR1 plays a key role in ethylene perception and regulation of downstream MdAAT2 gene expression during poststorage. Ester compounds and concentrations differed in peels treated with different signal molecules, indicating that regulation of the pathway upstream of straight-chain ester biosynthesis depended on the regulation of lipoxygenase (LOX) and alcohol dehydrogenase (ADH) activity by SA, ETH, and MeJA during poststorage ripening.
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PMID:Salicylic acid, ethephon, and methyl jasmonate enhance ester regeneration in 1-MCP-treated apple fruit after long-term cold storage. 1671 11

The expression of LeATL6, an ortholog of Arabidopsis ATL6 that encodes a RING-H2 finger protein, was induced in tomato roots treated with a cell wall protein fraction (CWP) elicitor of the biocontrol agent Pythium oligandrum. The LeATL6 protein was expressed as a fusion protein with a maltose-binding protein (MBP) in Escherichia coli, and it catalyzed the transfer of ubiquitin to the MBP moiety on incubation with ubiquitin, the ubiquitin-activating enzyme E1, and the ubiquitin-conjugating enzyme E2; this indicated that LeATL6 represents ubiquitin ligase E3. LeATL6 expression also was induced by elicitor treatment of jail-1 mutant tomato cells in which the jasmonic acid (JA)-mediated signaling pathway was impaired; however, JA-dependent expression of the basic PR-6 and TPI-1 genes that encode proteinase inhibitor II and I, respectively, was not induced in elicitor-treated jail-1 mutants. Furthermore, transient overexpression of LeATL6 under the control of the Cauliflower mosaic virus 35S promoter induced the basic PR6 and TPI-1 expression in wild tomato but not in the jail-1 mutant. In contrast, LeATL6 overexpression did not activate salicylic acid-responsive acidic PR-1 and PR-2 promoters in wild tomato. These results indicated that elicitor-responsive LeATL6 probably regulates JA-dependent basic PR6 and TPI-1 gene expression in tomato. The LeATL6-associated ubiquitin/proteasome system may contribute to elicitor-activated defense responses via a JA-dependent signaling pathway in plants.
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PMID:The LeATL6-associated ubiquitin/proteasome system may contribute to fungal elicitor-activated defense response via the jasmonic acid-dependent signaling pathway in tomato. 1724 24

Arabidopsis gain-of-resistance mutants, which show HR-like lesion formation and SAR-like constitutive defense responses, were used well as tools to unravel the plant defense mechanisms. We have identified a novel mutant, designated constitutive expresser of PR genes 30 (cpr30), that exhibited dwarf morphology, constitutive resistance to the bacterial pathogen Pseudomonas syringae and the dramatic induction of defense-response gene expression. The cpr30-conferred growth defect morphology and defense responses are dependent on ENHANCED DISEASE SUSCEPTIBILITY 1 (EDS1), PHYTOALEXIN DEFICIENT 4 (PAD4), and NONRACE-SPECIFIC DISEASE RESISTANCE 1 (NDR1). Further studies demonstrated that salicylic acid (SA) could partially account for the cpr30-conferred constitutive PR1 gene expression, but not for the growth defect, and that the cpr30-conferred defense responses were NPR1 independent. We observed a widespread expression of CPR30 throughout the plant, and a localization of CPR30-GFP fusion protein in the cytoplasm and nucleus. As an F-box protein, CPR30 could interact with multiple Arabidopsis-SKP1-like (ASK) proteins in vivo. Co-localization of CPR30 and ASK1 or ASK2 was observed in Arabidopsis protoplasts. Based on these results, we conclude that CPR30, a novel negative regulator, regulates both SA-dependent and SA-independent defense signaling, most likely through the ubiquitin-proteasome pathway in Arabidopsis.
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PMID:An F-box gene, CPR30, functions as a negative regulator of the defense response in Arabidopsis. 1968 97

In plants, resistance to necrotrophic pathogens depends on the interplay between different hormone systems, such as those regulated by salicylic acid (SA), jasmonic acid (JA), ethylene, and abscisic acid. Repression of auxin signaling by the SA pathway was recently shown to contribute to antibacterial resistance. Here, we demonstrate that Arabidopsis auxin signaling mutants axr1, axr2, and axr6 that have defects in the auxin-stimulated SCF (Skp1-Cullin-F-box) ubiquitination pathway exhibit increased susceptibility to the necrotrophic fungi Plectosphaerella cucumerina and Botrytis cinerea. Also, stabilization of the auxin transcriptional repressor AXR3 that is normally targeted for removal by the SCF-ubiquitin/proteasome machinery occurs upon P. cucumerina infection. Pharmacological inhibition of auxin transport or proteasome function each compromise necrotroph resistance of wild-type plants to a similar extent as in non-treated auxin response mutants. These results suggest that auxin signaling is important for resistance to the necrotrophic fungi P. cucumerina and B. cinerea. SGT1b (one of two Arabidopsis SGT1 genes encoding HSP90/HSC70 co-chaperones) promotes the functions of SCF E3-ubiquitin ligase complexes in auxin and JA responses and resistance conditioned by certain Resistance (R) genes to biotrophic pathogens. We find that sgt1b mutants are as resistant to P. cucumerina as wild-type plants. Conversely, auxin/SCF signaling mutants are uncompromised in RPP4-triggered resistance to the obligate biotrophic oomycete, Hyaloperonospora parasitica. Thus, the predominant action of SGT1b in R gene-conditioned resistance to oomycetes appears to be at a site other than assisting SCF E3-ubiquitin ligases. However, genetic additivity of sgt1b axr1 double mutants in susceptibility to H. parasitica suggests that SCF-mediated ubiquitination contributes to limiting biotrophic pathogen colonization once plant-pathogen compatibility is established.
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PMID:Repression of the auxin response pathway increases Arabidopsis susceptibility to necrotrophic fungi. 1982 56

The peptide derivative syringolin A, a product of a mixed nonribosomal peptide and polyketide synthetase, is secreted by certain strains of the phytopathogenic bacterium Pseudomonas syringae pv. syringae. Syringolin A was shown to be a virulence factor for P. syringae pv. syringae B728a because disease symptoms on its host Phaseolus vulgaris (bean) were greatly reduced upon inoculation with syringolin A-negative mutants. Syringolin A's mode of action was recently shown to be irreversible proteasome inhibition. Here, we report that syringolin A-producing bacteria are able to open stomata and, thus, counteract stomatal innate immunity in bean and Arabidopsis. Syringolin A-negative mutants, which induce stomatal closure, can be complemented by exogenous addition of not only syringolin A but also MG132, a well-characterized and structurally unrelated proteasome inhibitor. This demonstrates that proteasome activity is crucial for guard cell function. In Arabidopsis, stomatal immunity was salicylic acid (SA)-dependent and required NPR1, a key regulator of the SA-dependent defense pathway whose proteasome-dependent turnover has been reported to be essential for its function. Thus, elimination of NPR1 turnover through proteasome inhibition by syringolin A is an attractive hypothesis to explain the observed inhibition of stomatal immunity by syringolin A.
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PMID:Pseudomonas syringae virulence factor syringolin A counteracts stomatal immunity by proteasome inhibition. 2083 8


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