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At least 19 recordsLinked to original sources
PubMed2005

Concordant evolution of trichothecene 3-O-acetyltransferase and an rDNA species phylogeny of trichothecene-producing and non-producing fusaria and other ascomycetous fungi.

The cereal pathogen Fusarium graminearum species complex (e.g. Fusarium asiaticum, previously referred to as F. graminearum lineage 6) produces the mycotoxin trichothecene in infected grains. The fungus has a gene for self-defence, Tri101, which is responsible for 3-O-acetylation of the trichothecene skeleton in the biosynthetic pathway. Recently, trichothecene non-producers Fusarium oxysporum and Fusarium fujikuroi (teleomorph Gibberella fujikuroi) were shown to have both functional (Tri201) and non-functional (pseudo-Tri101) trichothecene 3-O-acetyltransferase genes in their genome. To gain insight into the evolution of the trichothecene genes in Gibberella species, the authors examined whether or not other (pseudo-)biosynthesis-related genes are found near Tri201. However, sequence analysis of a 12 kb region containing Tri201 did not result in identification of additional trichothecene (pseudo-)genes in F. oxysporum. In a further attempt to find other trichothecene (pseudo-)genes from the non-producer, the authors examined whether or not the non-trichothecene genes flanking the ends of the core trichothecene gene cluster (i.e. the Tri5 cluster) comprise a region of synteny in Gibberella species. However, it was not possible to isolate trichothecene (pseudo-)genes from F. oxysporum (in addition to the previously identified pseudo-Tri101), because synteny was not observed for this region in F. asiaticum and F. oxysporum. In contrast to this unsuccessful identification of additional trichothecene (pseudo-)genes in the non-producer, a functional trichothecene 3-O-acetyltransferase gene could be identified in fusaria other than Gibberella: Fusarium decemcellulare and Fusarium solani; and in an ascomycete from a different fungal genus, Magnaporthe grisea. Together with the recent functional identification of Saccharomyces cerevisiae ScAYT1, these results are suggestive of a different evolutionary origin for the trichothecene 3-O-acetyltransferase gene from other biosynthesis pathway genes. The phylogeny of the 3-O-acetyltransferase was mostly concordant with the rDNA species phylogeny of these ascomycetous fungi.

Acetyltransferases↗
PubMed2003

Relationship of trichothecene structure to COX-2 induction in the macrophage: selective action of type B (8-keto) trichothecenes.

The trichothecene mycotoxin deoxynivalenol (DON, vomitoxin), when at partially cytotoxic concentrations, induces cyclooxygenase-2 (COX-2) expression by promoting transcriptional activity and mRNA stability via mitogen-activated protein kinase (MAPK) signaling pathways. The purpose of this study was to test the hypothesis that trichothecenes differentially affect COX-2 gene expression and that these effects were related to MAPK activation. Representative members of the three major trichothecene families (A, B, and D) were compared for their capacity to induce COX-2 in the RAW 264.7 murine macrophage cell line. When cells were treated with concentrations that inhibited the 3-(4,5-di-methylthizol-2-yl)-2,5 diphenyl tetrazolium bromide (MTT) viability response by 20% (IC20), Type B trichothecenes including DON, 15-acetyl-DON, 3-acetyl-DON, and fusarenon-X were found to be effective inducers of COX-2 mRNA expression, whereas equitoxic Type A and Type D trichothecenes had markedly less effects. To compare effects of COX-2 gene transactivation and mRNA stabilization, luciferase reporter vectors containing 5'-promoter or 3'-untranslated regions of the gene, respectively, were transfected into RAW 264.7 cells and the effects of various trichothecenes on luciferase activities were measured. Type B but not Type A or D toxins at concentrations up to the MTT IC50 enhanced luciferase activities, indicating preferential COX-2 transcriptional activation and mRNA stabilization by this trichothecene subset. At their respective IC20s, Type B trichothecenes also significantly activated the three major MAPK families, whereas Type A and D did not. Blocking ERK and p38 with chemical inhibitors significantly suppressed Type B-induced COX-2 expression. Although JNK reportedly contributes to COX-2 expression in the other signaling models, transfection with the dominant negative JNK vector did not diminish the COX-2 expression. Taken together, Type B trichothecenes selectively enhanced transcription and stabilization of the COX-2 gene, and this was mediated by the ERK 1/2 and p38 signaling pathways. Selective action on COX-2 might contribute to unique pathologic manifestations associated with Type B trichothecene-mediated immunotoxicity.

Animals↗
PubMed1986

Mass spectral investigations on trichothecene mycotoxins. I. Application of negative ion chemical ionization techniques for the simultaneous and accurate analysis of simple trichothecenes in picogram levels.

A fast and sensitive gas chromatographic/negative ion chemical ionization mass spectrometric method for the simultaneous detection and quantification of several simple trichothecene mycotoxins and related molecules with good precision has been developed. The method consists of the conversion of the polar trichothecenes into their volatile and stable heptafluorobutyryl esters, followed by gas chromatographic/mass spectrometric analysis of the derivatives. The derivatives were ionized under chemical ionization conditions and the negative ions were monitored. The samples were screened for the presence of trichothecenes by monitoring one characteristic ion by selected ion monitoring for each analyte. The detected compounds were confirmed by monitoring 5-6 characteristic ions by selected ion monitoring whenever the amount of analyte present was insufficient to obtain a full scan negative ion chemical ionization mass spectrum. Two semi-synthetic trichothecenes, 4-deoxyverrucarol and 16-hydroxyverrucarol, were investigated and found to be adequate internal standards both for detection and quantification of these toxic compounds. Femtogram and low picogram (1-5 pg) quantities of these compounds could be detected and confirmed, respectively, by this procedure. A short clean-up procedure using Sep-Pak (silica gel) cartridges was developed and found to be applicable for the analysis of some real samples. Several spiked and real samples were analysed by this method, with excellent sensitivity and precision.

Chemical Phenomena↗
PubMed1978

Metabolism of trichothecene mycotoxins. II. Substrate specificity of microsomal deacetylation of trichothecenes.

The substrate specificity of microsomal nonspecific carboxyesterase [EC 3.1.1.1] from rabbit and rat livers was studied in vitro by using seven (A)-type and six (B)-type 12,13-epoxytrichothecene mycotoxins. The C-4 acetyl residues of diacetoxyscirpenol, T-2 toxin, monoacetylnivalenol (fusarenon-X), and diacetylnivalenol were selectively hydrolyzed by the microsomal esterase to yield the corresponding C-4-deacetylated metabolites: monoacetoxyscirpenol, HT-2 toxin, nivalenol, and 15-acetylnivalenol, respectively. The C-3 acetyl group of monoacetyldeoxynivalenol and the C-8 acetyl group of tetraacetoxyscirpen were also deacetylated. Triacetoxyscirpen gave rise to two unidentified metabolites, which may include a C-4-deacetylated product. 8-Hydroxydiacetoxyscirpenol (neosolaniol), HT-2 toxin, acetyl-T-2 toxin and tetraacetylnivalenol were unaffected by this type of hydrolysis. It follow from these results that the C-4 acetyl residue is hydrolyzed by the microsomal carboxyesterase and substituents at C-3 and C-8 contribute to the selective enzymatic hydrolysis of the C-4 acetyl residue of trichothecenes. Kinetic analysis showed that rabbit microsomal esterase possessed a high affinity for (A)-type trichothecenes such as T-2 toxin and diacetoxyscirpenol, and that of rat microsomes possessed a high affinity for (B)-type trichothecenes such as monoacetylnivalenol (fusarenon-X). The significance of this specific deacetylation reaction is discussed in relation to the biological activity of the trichothecene derivatives as revealed by their inhibitory effect on protein synthesis in rabbit reticulocytes.

Animals↗
PubMed1989

Investigation on trichothecene-stimulated lipid peroxidation and toxic effects of trichothecenes in animals.

Three experiments were performed with mice intoxicated with trichothecene-contamined feed or directly into the stomach. Lipid peroxidation was estimated by the TBA value from liver samples, but since such a test seldom provided reliable results, lipid hydroperoxides and total carbonyl were also analyzed. The formation of aldehydes and ketones was compared in vivo and in vitro. The same investigations were conducted on chickens, rainbow trouts and numerous fur animals suspected of chronic intoxication by trichothecenes. The vitamin A concentration was used as a parameter to detect alterations caused in chickens by trichothecenes. Our investigation provided evidence that lipid peroxidation is associated with trichothecene poisoning. The T-2 toxin, even in small concentrations, seems to induce strong lipid peroxidation. When DON and 3-AcDON were given together at a dosage of 180 micrograms/kg feed, 1 week's feeding caused clear lipid peroxidation in mice. Particular attention should be paid to the fact that mycotoxins may already be present in the feed before any experiment is conducted.

Animals↗
PubMed1989

Mass spectral investigations on trichothecene mycotoxins. VII. Liquid chromatographic-thermospray mass spectrometric analysis of macrocyclic trichothecenes.

Thermally labile, polar toxic roridins and biologically active, isomeric baccharinoids were separated on a reversed-phase high-performance liquid chromatography column and effectively ionized under thermospray ionization conditions. The mass spectra indicated the formation of corresponding molecular ion-ammonium adducts in great abundance. Experiments designed for monitoring specific ions of these analytes at predesignated intervals were utilized for the accurate analysis of these macrocyclic trichothecenes in real, crude samples. A synthetically modified macrocyclic trichothecene, 8-ketoverrucarin A, was used as the internal standard for the detection and quantification of these compounds. Minimum detectable limits, during this first reported method for the unambiguous analysis of these structurally related macrocyclic trichothecenes, were determined to be 2-5 ng.

Chemical Phenomena↗
PubMed1986

Mass spectral investigations on trichothecene mycotoxins. III. Synthesis, characterization and applications of pentafluoropropionyl and trifluoroacetyl esters of simple trichothecenes.

The pentafluoropropionyl, (PFP) and trifluoroacetyl (TFA) esters of several naturally occurring and synthetically modified simple trichothecenes were synthesized in nanogram amounts and characterized. Optimum conditions for the gas chromatographic (GC) separation of these derivatives and their analysis by negative ion chemical ionization (NICI) mass spectrometric technique were determined. These perfluoroacyl derivatives under the NICI conditions undergo limited but characteristic fragmentations similar to the fragmentations of heptafluorobutyryl esters of trichothecenes under the same conditions. Characteristic ions for the specific detection and accurate quantification of these PFP and TFA derivatives were chosen. Preliminary results indicated that the PFP derivatives are better suited for the analysis of simple trichothecenes by GC-NICI-MS technique. Ultra trace (0.5-2.0 pg) amounts of these PFP derivatives were detected by the developed procedure.

Fluorocarbons↗
PubMedDate not supplied

Mass spectral investigations on trichothecene mycotoxins. II. Detection and quantitation of macrocyclic trichothecenes by gas chromatography/negative ion chemical ionization mass spectrometry.

A general, sensitive gas chromatographic/negative ion chemical ionization mass spectrometric (GC/NICIMS) method of analysis was developed for the detection and quantitation of several polar, thermally labile, toxic macrocyclic trichothecenes. The procedure involves the conversion of the molecules to their corresponding alcohols (verrucarols) by alkaline hydrolysis, followed by derivatization of the hydrolysate with heptafluorobutyrylimidazole and analysis by GC/MS technique under negative ion chemical ionization conditions. Nanogram (250 ng) quantities of several macrocyclic trichothecenes with different verrucarol and ester moieties were analyzed successfully with good precision by this procedure. The method was applicable for the accurate determination of at least low ppb levels of these macrocyclic trichothecenes in environmental samples, such as fungal products, fermentation broths, and plant samples. This is the first reported, well developed, sensitive, and applicable method for the detection and quantitation of these compounds in naturally occurring samples.

Fermentation↗
PubMed1989

Mass spectral investigations on trichothecene mycotoxins. VIII--Thermospray ionization and collisionally activated dissociation of macrocyclic trichothecenes.

Several structurally similar, biologically active macrocyclic trichothecenes were ionized under thermospray conditions followed by collisionally activated dissociation of the ammonium adducts. Most of the observed daughter ions were formed by bond cleavage at the exocyclic ester bridges. Compounds with similar ester bridges formed several common daughter ions and underwent similar neutral losses. Fragmentation pathways proposed for the dissociation of the adducts were confirmed from the corresponding neutral loss spectra. Simple experiments designed for the sequential monitoring of the characteristic daughter ions were used for the rapid, direct and accurate analysis of macrocyclic trichothecenes in real samples. The primary drawback of the method is its inability to distinguish between isomers.

Chemical Phenomena↗
PubMed1997

Accumulation of Trichothecenes in Liquid Cultures of a Fusarium sporotrichioides Mutant Lacking a Functional Trichothecene C-15 Hydroxylase.

A mutant strain of Fusarium sporotrichioides NRRL 3299 produced by disruption of Tri11, a gene encoding a cytochrome P-450 monooxygenase, was shown to be altered in its ability to biosynthesize T-2 toxin. This mutant strain produced four trichothecenes that were not observed in cultures of the parent strain. The compounds were identified as isotrichodermin, 8-hydroxyisotrichodermin, 8-hydroxyisotrichodermol, and 3,4,8-trihydroxytricothecene on the basis of their nuclear magnetic resonance and mass spectra. This is the first report of these 8-hydroxytrichothecenes as metabolites of F. sporotrichioides. The accumulation of isotrichodermin and the results of whole-cell feeding experiments with a Tri11(sup-) strain confirm that oxygenation of C-15 is blocked.

Journal Article↗
PubMed1989

Production of trichothecene and non-trichothecene mycotoxins by Fusarium species isolated from maize in Minnesota.

Eighty-two cultures of Fusarium species isolated in 1986 from moldy maize in Minnesota were each cultured on rice for 4 weeks and found to produce the following mycotoxins: F. graminearum isolates, deoxynivalenol (DON, 4-225 micrograms/g), 3-acetyldeoxynivalenol (3-ADON, 2-4 micrograms/g), 15-acetyldeoxynivalenol (15-ADON, 1-35 micrograms/g) and zearalenone (ZEA, 5-4350 micrograms/g); F. moniliforme, fusarin C (detectable amounts to 1000 micrograms/g); F. moniliforme, F. oxysporum, F. proliferatum and F. subglutinans isolates, moniliformin (15-6775 micrograms/g); F. moniliforme, F. proliferatum, and F. subglutinans isolates, fusaric acid (detectable amounts). Other mycotoxins screened for in each rice sample and not detected were T-2 toxin, HT-2 toxin, neosolaniol, T-2 tetraol, nivalenol, fusarenon-X, scirpenols, alpha and beta trans-zearalenols, wortmannin, and fusarochromanone. The rat feeding bioassay indicated that other, unidentified toxins may be present.

Culture Media↗
PubMed1998

Characterization of the gene cluster for biosynthesis of macrocyclic trichothecenes in Myrothecium roridum.

Macrocyclic trichothecenes are toxic sesquiterpenoids that are produced by certain fungi and plants. The unique structural features of macrocyclic trichothecenes result in increased toxicity relative to other trichothecene structural types. Here we report the sequences and relative locations of the MRTRI5, MRTRI6, and MRTRI4 genes in the biosynthetic pathway for macrocyclic trichothecenes in Myrothecium roridum. The deduced sequences of the products of MRTRI5 and MRTRI4 display overall identities of 75 and 63%, respectively, with the corresponding proteins in Fusarium sporotrichioides. Based on sequence comparisons, MRTRI5 encodes the enzyme trichodiene synthase, which has been shown to catalyze the first step in the trichothecene pathways of Fusarium and Trichothecium species. MRTRI6 encodes a transcription factor (392 amino acids) required for pathway gene expression, and the predicted MRTRI4 product (533 amino acids) is a cytochrome P450 monooxygenase responsible for the initial oxygenation step in the pathway. The sizes of the predicted products of MRTRI5 and MRTRI4 show good agreement with their apparent counterparts in the Fusarium pathway; however, the protein specified by MRTRI6 is almost twice the size of its putative homolog in F. sporotrichioides. Only the C-terminal 124 residues of MRTRI6, containing the proposed Cys2His2 zinc finger motifs, show significant similarity (65% identity) to the TRI6 sequence in F. sporotrichioides. MRTRI4 can successfully complement a TRI4-mutant in F. sporotrichioides, although the resulting trichothecene profile differed from that observed in wild-type strains. Complemented mutants accumulated low levels of T-2 toxin, in addition to sambucinol, deoxysambucinol, and the pathway intermediates trichothecene and isotrichodiol. Mapping data indicate that the genes of the macrocyclic trichothecene pathway in M. roridum are clustered, but that their organization and orientation differ markedly from those of the trichothecene gene cluster found in F. sporotrichioides. These results show that the biosynthetic pathways for macrocyclic trichothecenes are closely related to other trichothecene pathways and that the evolution of gene clusters for the biosynthesis of natural products in fungi can involve significant rearrangements.

Amino Acid Sequence↗
PubMed2000

Apoptosis induction by the satratoxins and other trichothecene mycotoxins: relationship to ERK, p38 MAPK, and SAPK/JNK activation.

The satratoxins are members of the trichothecene mycotoxin family that are produced by the fungus Stachybotrys and that have been etiologically associated with building-related health problems. The purpose of this study was to relate cytotoxic and apoptotic capacities of satratoxins and other trichothecenes to the activation of three groups of mitogen-activated protein kinases (MAPKs) (extracellular signal-regulated protein kinase (ERK), p38 MAPK, and stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK)). Two myeloid models, RAW 264.7 murine macrophage and U937 human leukemic cells were used. Upon evaluating representative trichothecenes in the 3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyl tetrazolium bromide (MTT) cleavage assay, cytotoxicity was evident according to the following rank order: satratoxin G, roridin A, and verrucarin A > T-2 toxin, satratoxin F, H > nivalenol, and vomitoxin. Comparable results were found when measuring trichothecene-mediated apoptosis using DNA fragmentation and fluorescence microscopy assays, thus suggesting that cytotoxicity was mediated through an apoptotic process. Assessment of MAPK activation using Western blot analysis revealed that trichothecenes activated not only SAPK/JNK and p38 MAPK but also ERK. Activation of MAPKs by satratoxins and other trichothecenes correlated with and preceded apoptosis. The concentration of satratoxin G sufficient for protein synthesis inhibition correlated with that required for apoptosis and activation of all three MAPKs. Cycloheximide had similar effects to trichothecenes, suggesting that ribosome binding or protein synthesis inhibition may play roles in MAPK activation and apoptosis induction. Apoptosis induction by satratoxin G and vomitoxin was markedly enhanced when ERK activation was selectively inhibited by ERK-specific inhibitor PD98059, thus indicating a negative role for ERK. Inhibition of p38 MAPK activity with the p38-specific inhibitor SB203580 had no effect on apoptosis induction by the highly toxic satratoxin G. However, SB203580 moderately inhibited apoptosis induction by the less toxic trichothecene vomitoxin, thus implying a partial role of p38 MAPK in trichothecene-induced apoptosis. The results suggest that the satratoxins are among the most potent trichothecenes and that MAPKs may play integral roles in the diverse toxic manifestations of these mycotoxins.

Animals↗
PubMed1999

TRI12, a trichothecene efflux pump from Fusarium sporotrichioides: gene isolation and expression in yeast.

Many of the genes involved in trichothecene toxin biosynthesis in Fusarium sporotrichioides are present within a gene cluster. Here we report the complete sequence for TRI12, a gene encoding a trichothecene efflux pump that is located within the trichothecene gene cluster of F. sporotrichioides. TRI12 encodes a putative polypeptide of 598 residues with sequence similarities to members of the major facilitator superfamily (MFS) and is predicted to contain 14 transmembrane-spanning segments. Disruption of TRI12 results in both reduced growth on complex media and reduced levels of trichothecene production. Growth of tri12 mutants on trichothecene-containing media is inhibited, suggesting that TRI12 may play a role in F. sporotrichioides self-protection against trichothecenes. Functional analysis of TRI12 was performed by expressing it in yeast strains that were co-transformed with a gene (TRI3) encoding a trichothecene 15-O-acetyltransferase. In the presence of the TRI3 substrate, 15-decalonectrin, cultures of yeast strains carrying TRI12 and TRI3 accumulated much higher levels of the acetylated product, calonectrin, than was observed for strains carrying TRI3 alone. PDR5, a transporter of the ABC superfamily, which is known to mediate trichothecene resistance in yeast, increased calonectrin accumulation in TRI12/TRI3 yeast strains but not in TRI3 strains. These results confirm the involvement of TRI12 in the trichothecene efflux associated with toxin biosynthesis, and demonstrate the usefulness of yeast as a host system for studies of MFS-type transporters.

Amino Acid Sequence↗
PubMed1999

Trichothecene mycotoxins trigger a ribotoxic stress response that activates c-Jun N-terminal kinase and p38 mitogen-activated protein kinase and induces apoptosis.

The trichothecene family of mycotoxins inhibit protein synthesis by binding to the ribosomal peptidyltransferase site. Inhibitors of the peptidyltransferase reaction (e.g. anisomycin) can trigger a ribotoxic stress response that activates c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinases, components of a signaling cascade that regulates cell survival in response to stress. We have found that selected trichothecenes strongly activate JNK/p38 kinases and induce rapid apoptosis in Jurkat T cells. Although the ability of individual trichothecenes to inhibit protein synthesis and activate JNK/p38 kinases are dissociable, both effects contribute to the induction of apoptosis. Among trichothecenes that strongly activate JNK/p38 kinases, induction of apoptosis increases linearly with inhibition of protein synthesis. Among trichothecenes that strongly inhibit protein synthesis, induction of apoptosis increases linearly with activation of JNK/p38 kinases. Trichothecenes that inhibit protein synthesis without activating JNK/p38 kinases inhibit the function (i.e. activation of JNK/p38 kinases and induction of apoptosis) of apoptotic trichothecenes and anisomycin. Harringtonine, a structurally unrelated protein synthesis inhibitor that competes with trichothecenes (and anisomycin) for ribosome binding, also inhibits the activation of JNK/p38 kinases and induction of apoptosis by trichothecenes and anisomycin. Taken together, these results implicate the peptidyltransferase site as a regulator of both JNK/p38 kinase activation and apoptosis.

Anisomycin↗
PubMed2006

Toxigenic Fusarium spp. as determinants of trichothecene mycotoxins in settled grain dust.

Trichothecenes are immunosuppressive mycotoxins produced mainly by Fusarium spp. and often are detected as natural contaminants of grain and other agricultural products. Exposure to trichothecenes through inhalation during grain work may represent possible health risks for grain farmers. We aimed, therefore, to investigate the level of Fusarium spp. and trichothecenes in settled grain dust collected during work on 92 Norwegian farms. Mycotoxins were determined by gas chromatography-mass spectrometry, whereas the Fusarium spp. were identified and quantified both by species-specific semiquantitative polymerase chain reaction (PCR) and by cultivation. All potential trichothecene-producing molds in the grain dust were quantified using a PCR assay specific for tri5, the gene coding for trichodiene synthase that catalyzes the first step in the trichothecene biosynthesis. We performed correlation analysis between mold-DNA and mycotoxins to assess whether the PCR-detected DNA could be used as indicators of the mycotoxins. The methodological problem of detecting small amounts of airborne mycotoxins during grain work may then be avoided. Whereas the trichothecene-producing Fusarium species in grain dust could not be identified or quantified to a sufficient extent by cultivation, all investigated Fusarium spp. could be specifically detected by PCR and quantified from the DNA agarose gel band intensities. Furthermore, we observed a strong correlation between the trichothecenes HT-2 toxin (HT-2) or T-2 toxin (T-2) and DNA specific for tri5 (r = 0.68 for HT-2 and r = 0.50 for T-2; p < 0.001), F. langsethiae (r = 0.77 for HT-2 and r = 0.59 for T-2; p < 0.001), or F. poae (r = 0.41 for HT-2 and r = 0.35 for T-2; p < 0.001). However, only a moderate correlation was observed between the trichothecene deoxynivalenol (DON) and the combination of its producers, F. culmorum and F. graminearum (r = 0.24, p = 0.02), and no significant correlation was observed between DON and tri5. PCR clearly improved the detection of toxigenic Fusaria as potential sources of health risks for farmers inhaling grain dust during work, but the use of Fusarium-DNA as indicators for trichothecenes should be used cautiously.

DNA, Fungal↗
PubMed2006

Fusarium phytotoxin trichothecenes have an elicitor-like activity in Arabidopsis thaliana, but the activity differed significantly among their molecular species.

Phytopathogenic fungi such as Fusarium spp. synthesize trichothecene family phytotoxins. Although the type B trichothecene, deoxynivalenol (DON), is thought to be a virulence factor allowing infection of plants by their trichothecene-producing Fusarium spp., little is known about effects of trichothecenes on the defense response in host plants. Therefore, in this article, we investigated these effects of various trichothecenes in Fusarium-susceptible Arabidopsis thaliana. Necrotic lesions were observed in Arabidopsis leaves infiltrated by 1 microM type A trichothecenes such as T-2 toxin. Trichothecene-induced lesions exhibited dead cells, callose deposition, generation of hydrogen peroxide, and accumulation of salicylic acids. Moreover, infiltration by trichothecenes caused rapid and prolonged activation of two mitogen-activated protein kinases and induced expression of both PR-1 and PDF1.2 genes. Thus, type A trichothecenes trigger the cell death by activation of an elicitor-like signaling pathway in Arabidopsis. Although DON did not have such an activity even at 10 microM, translational inhibition by DON was observed at concentrations above 5 microM. These results suggested that DON is capable of inhibiting translation in Arabidopsis cells without induction of the elicitor-like signaling pathway.

Arabidopsis↗