scholarly journals The Combined Action of ENHANCED DISEASE SUSCEPTIBILITY1, PHYTOALEXIN DEFICIENT4, and SENESCENCE-ASSOCIATED101 Promotes Salicylic Acid-Mediated Defenses to Limit Fusarium graminearum Infection in Arabidopsis thaliana

2015 ◽  
Vol 28 (8) ◽  
pp. 943-953 ◽  
Author(s):  
Ragiba Makandar ◽  
Vamsi J. Nalam ◽  
Zulkarnain Chowdhury ◽  
Sujon Sarowar ◽  
Guy Klossner ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Salicylic Acid ◽  
Fusarium Graminearum ◽  
Response Regulator ◽  
Constitutive Expression ◽  
Catalytic Triad ◽  
Head Blight ◽  
Molecular Configuration ◽  
Combined Action ◽  
Arabidopsis Defense

Fusarium graminearum causes Fusarium head blight (FHB) disease in wheat and other cereals. F. graminearum also causes disease in Arabidopsis thaliana. In both Arabidopsis and wheat, F. graminearum infection is limited by salicylic acid (SA) signaling. Here, we show that, in Arabidopsis, the defense regulator EDS1 (ENHANCED DISEASE SUSCEPTIBILITY1) and its interacting partners, PAD4 (PHYTOALEXIN-DEFICIENT4) and SAG101 (SENESCENCE-ASSOCIATED GENE101), promote SA accumulation to curtail F. graminearum infection. Characterization of plants expressing the PAD4 noninteracting eds1L262P indicated that interaction between EDS1 and PAD4 is critical for limiting F. graminearum infection. A conserved serine in the predicted acyl hydrolase catalytic triad of PAD4, which is not required for defense against bacterial and oomycete pathogens, is necessary for limiting F. graminearum infection. These results suggest a molecular configuration of PAD4 in Arabidopsis defense against F. graminearum that is different from its defense contribution against other pathogens. We further show that constitutive expression of Arabidopsis PAD4 can enhance FHB resistance in Arabidopsis and wheat. Taken together with previous studies of wheat and Arabidopsis expressing salicylate hydroxylase or the SA-response regulator NPR1 (NON-EXPRESSER OF PR GENES1), our results show that exploring fundamental processes in a model plant provides important leads to manipulating crops for improved disease resistance.

scholarly journals Facilitation of Fusarium graminearum Infection by 9-Lipoxygenases in Arabidopsis and Wheat

2015 ◽  
Vol 28 (10) ◽  
pp. 1142-1152 ◽  
Author(s):  
Vamsi J. Nalam ◽  
Syeda Alam ◽  
Jantana Keereetaweep ◽  
Barney Venables ◽  
Dehlia Burdan ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Salicylic Acid ◽  
Disease Resistance ◽  
Jasmonic Acid ◽  
Fusarium Graminearum ◽  
Head Blight ◽  
Enhanced Resistance ◽  
Susceptibility Factors ◽  
Ja Signaling ◽  
Important Disease

Fusarium graminearum causes Fusarium head blight, an important disease of wheat. F. graminearum can also cause disease in Arabidopsis thaliana. Here, we show that the Arabidopsis LOX1 and LOX5 genes, which encode 9-lipoxygenases (9-LOXs), are targeted during this interaction to facilitate infection. LOX1 and LOX5 expression were upregulated in F. graminearum–inoculated plants and loss of LOX1 or LOX5 function resulted in enhanced disease resistance in the corresponding mutant plants. The enhanced resistance to F. graminearum infection in the lox1 and lox5 mutants was accompanied by more robust induction of salicylic acid (SA) accumulation and signaling and attenuation of jasmonic acid (JA) signaling in response to infection. The lox1- and lox5-conferred resistance was diminished in plants expressing the SA-degrading salicylate hydroxylase or by the application of methyl-JA. Results presented here suggest that plant 9-LOXs are engaged during infection to control the balance between SA and JA signaling to facilitate infection. Furthermore, since silencing of TaLpx-1 encoding a 9-LOX with homology to LOX1 and LOX5, resulted in enhanced resistance against F. graminearum in wheat, we suggest that 9-LOXs have a conserved role as susceptibility factors in disease caused by this important fungus in Arabidopsis and wheat.

scholarly journals Fusarium graminearum ATP-Binding Cassette Transporter Gene FgABCC9 Is Required for Its Transportation of Salicylic Acid, Fungicide Resistance, Mycelial Growth and Pathogenicity towards Wheat

2018 ◽  
Vol 19 (8) ◽  
pp. 2351 ◽  
Author(s):  
Peng-Fei Qi ◽  
Ya-Zhou Zhang ◽  
Cai-Hong Liu ◽  
Jing Zhu ◽  
Qing Chen ◽  
...  
Keyword(s):  
Salicylic Acid ◽  
Fusarium Graminearum ◽  
Mycelial Growth ◽  
Tertiary Structure ◽  
Severe Disease ◽  
Atp Binding ◽  
Head Blight ◽  
Transporter Family ◽  
Wide Range ◽  
Atp Binding Cassette

ATP-binding cassette (ABC) transporters hydrolyze ATP to transport a wide range of substrates. Fusarium graminearum is a major causal agent of Fusarium head blight, which is a severe disease in wheat worldwide. FgABCC9 (FG05_07325) encodes an ABC-C (ABC transporter family C) transporter in F. graminearum, which was highly expressed during the infection in wheat and was up-regulated by the plant defense hormone salicylic acid (SA) and the fungicide tebuconazole. The predicted tertiary structure of the FgABCC9 protein was consistent with the schematic of the ABC exporter. Deletion of FgABCC9 resulted in decreased mycelial growth, increased sensitivity to SA and tebuconazole, reduced accumulation of deoxynivalenol (DON), and less pathogenicity towards wheat. Re-introduction of a functional FgABCC9 gene into ΔFgABCC9 recovered the phenotypes of the wild type strain. Transgenic expression of FgABCC9 in Arabidopsis thaliana increased the accumulation of SA in its leaves without activating SA signaling, which suggests that FgABCC9 functions as an SA exporter. Taken together, FgABCC9 encodes an ABC exporter, which is critical for fungal exportation of SA, response to tebuconazole, mycelial growth, and pathogenicity towards wheat.

scholarly journals Major Facilitator Superfamily Transporter Gene FgMFS1 Is Essential for Fusarium graminearum to Deal with Salicylic Acid Stress and for Its Pathogenicity towards Wheat

2021 ◽  
Vol 22 (16) ◽  
pp. 8497
Author(s):  
Qing Chen ◽  
Lu Lei ◽  
Caihong Liu ◽  
Yazhou Zhang ◽  
Qiang Xu ◽  
...  
Keyword(s):  
Salicylic Acid ◽  
Fusarium Graminearum ◽  
Total Yield ◽  
Acid Stress ◽  
Major Facilitator Superfamily ◽  
Dimensional Structure ◽  
Transporter Gene ◽  
Loss Of Function ◽  
Head Blight ◽  
Major Facilitator

Wheat is a major staple food crop worldwide, due to its total yield and unique processing quality. Its grain yield and quality are threatened by Fusarium head blight (FHB), which is mainly caused by Fusarium graminearum. Salicylic acid (SA) has a strong and toxic effect on F. graminearum and is a hopeful target for sustainable control of FHB. F. graminearum is capable of efficientdealing with SA stress. However, the underlying mechanisms remain unclear. Here, we characterized FgMFS1 (FGSG_03725), a major facilitator superfamily (MFS) transporter gene in F. graminearum. FgMFS1 was highly expressed during infection and was upregulated by SA. The predicted three-dimensional structure of the FgMFS1 protein was consistent with the schematic for the antiporter. The subcellular localization experiment indicated that FgMFS1 was usually expressed in the vacuole of hyphae, but was alternatively distributed in the cell membrane under SA treatment, indicating an element of F. graminearum in response to SA. ΔFgMFS1 (loss of function mutant of FgMFS1) showed enhanced sensitivity to SA, less pathogenicity towards wheat, and reduced DON production under SA stress. Re-introduction of a functional FgMFS1 gene into ∆FgMFS1 recovered the mutant phenotypes. Wheat spikes inoculated with ΔFgMFS1 accumulated more SA when compared to those inoculated with the wild-type strain. Ecotopic expression of FgMFS1 in yeast enhanced its tolerance to SA as expected, further demonstrating that FgMFS1 functions as an SA exporter. In conclusion, FgMFS1 encodes an SA exporter in F. graminearum, which is critical for its response to wheat endogenous SA and pathogenicity towards wheat.

scholarly journals Transcript Abundance Responses of Resistance Pathways of Arabidopsis thaliana to Deoxynivalenol

2017 ◽  
Vol 2 (3) ◽  
pp. 154-161
Author(s):  
Jiazheng Yuan ◽  
Michelle Zhu ◽  
Khalid Meksem ◽  
Matt Geisler ◽  
Patrick Hart ◽  
...  
Keyword(s):  
Arabidopsis Thaliana ◽  
Fusarium Graminearum ◽  
Transcript Abundance ◽  
Triticum Aestivum L ◽  
Gibberella Zeae ◽  
Ear Rot ◽  
Head Blight ◽  
Soybean Roots ◽  
Stress Related Genes ◽  
Expressed Sequence

Mycotoxin deoxynivalenol (DON), produced by Gibberella zeae (Schwein.) Petch (teleomorph of Fusarium graminearum Schwabe) was known to be both a virulence factor in the pathogenesis of Triticum aestivum L. (wheat) and an inhibitor of Arabidopsis thaliana L. seed germination. Fusarium graminearum causes both Gibberella ear rot in maize (Zea mays L.) and Fusarium head blight (FHB) in wheat and barley. Arabidopsis thaliana was also a host for the related root rot pathogen F. virguliforme Aoki. A. thaliana seedling growth was reduced by the pathogen in a proportional response to increasing spore concentrations. Here, the changes in transcript abundances corresponding to 10,560 A. thaliana expressed sequence tags (ESTs) was compared with changes in 192 known plant defense and biotic/abiotic stress related genes in soybean roots after infestation with F. virguliforme. A parallel comparison with a set of resistance pathways involved in response to the DON toxicity in A. thaliana was performed. A. thaliana data was obtained from the AFGC depository. The variations of transcript abundances in Arabidopsis and soybean treated with pathogen suggest that both plants respond to the pathogen mainly by common, possibly global responses with some specific secondary metabolic pathways involved in defense. In contrast, DON toxin appeared to impact central metabolisms in Arabidopsis plants with significant alterations ranging from the protein metabolism to redox production. Several new putative resistance pathways involved in responding to both pathogen and DON infestation in soybean and A. thaliana were identified.

scholarly journals The vesicular trafficking system component MIN7 is required for minimizing Fusarium graminearum infection

2020 ◽  
Author(s):  
Ana K. Machado Wood ◽  
Vinay Panwar ◽  
Mike Grimwade-Mann ◽  
Tom Ashfield ◽  
Kim E. Hammond-Kosack ◽  
...  
Keyword(s):  
Innate Immunity ◽  
Arabidopsis Thaliana ◽  
Pseudomonas Syringae ◽  
Fusarium Graminearum ◽  
Fungal Pathogen ◽  
Vesicular Trafficking ◽  
Crop Plants ◽  
System Component ◽  
Head Blight ◽  
Wide Range

ABSTRACTPlants have developed intricate defense mechanisms, referred to as innate immunity, to defend themselves against a wide range of pathogens. Plants often respond rapidly to pathogen attack by the synthesis and delivery of various antimicrobial compounds, proteins and small RNA in membrane vesicles to the primary infection sites. Much of the evidence regarding the importance of vesicular trafficking in plant-pathogen interactions comes from the studies involving model plants whereas this process is relatively understudied in crop plants. Here we assessed whether the vesicular trafficking system components previously implicated in immunity in Arabidopsis thaliana play a role in the interaction with Fusarium graminearum, a fungal pathogen notoriously famous for its ability to cause Fusarium head blight (FHB) disease in wheat. Among the analyzed vesicular trafficking mutants, two independent T-DNA insertion mutants in the AtMin7 gene displayed a markedly enhanced susceptibility to F. graminearum. Earlier studies identified this gene, encoding an ARF-GEF protein, as a target for the HopM1 effector of the bacterial pathogen Pseudomonas syringae pv. tomato, which destabilizes AtMIN7 leading to its degradation and weakening host defenses. To test whether this key vesicular trafficking component may also contribute to defense in crop plants, we identified the candidate TaMin7 genes in wheat and knocked-down their expression through Virus induced gene silencing. Wheat plants in which TaMIN7 were silenced displayed significantly more FHB disease. This suggests that disruption of MIN7 function in both model and crop plants compromises the trafficking of innate immunity signals or products resulting in hyper-susceptibility to various pathogens.One sentence summaryDisruption of an ARF-GEF protein encoding gene AtMin7 in Arabidopsis thaliana and silencing of the orthologous gene in wheat result in hyper susceptibility to the fungal pathogen Fusarium graminearum.

scholarly journals Involvement of Salicylate and Jasmonate Signaling Pathways in Arabidopsis Interaction with Fusarium graminearum

2010 ◽  
Vol 23 (7) ◽  
pp. 861-870 ◽  
Author(s):  
Ragiba Makandar ◽  
Vamsi Nalam ◽  
Ratnesh Chaturvedi ◽  
Richard Jeannotte ◽  
Alexis A. Sparks ◽  
...  
Keyword(s):  
Fusarium Graminearum ◽  
Systemic Acquired Resistance ◽  
Acquired Resistance ◽  
Head Blight ◽  
Pathogenesis Related ◽  
Ja Signaling ◽  
Arabidopsis Defense ◽  
Sa Signaling ◽  
Dependent Mechanism

Fusarium graminearum is the principal causative agent of Fusarium head blight (FHB), a devastating disease of wheat and barley. This fungus can also colonize Arabidopsis thaliana. Disease resistance was enhanced in transgenic wheat and Arabidopsis plants that constitutively overexpress the NONEXPRESSOR OF PATHOGENESIS-RELATED GENES 1 (NPR1) gene, which regulates salicylic acid (SA) signaling and modulates the activation of jasmonic acid (JA)-dependent defenses. Here, we provide several lines of evidence that reveal an important role for SA and JA signaling in Arabidopsis defense against F. graminearum. SA level was elevated in fungus-inoculated leaves, and SA application and biologically activated systemic acquired resistance enhanced resistance. Furthermore, the disruption of SA accumulation and signaling in the sid2 mutant and NahG transgenic plant, and the npr1 and wrky18 mutants, respectively, resulted in heightened susceptibility to this fungus in leaves and inflorescence. JA signaling was activated in parallel with SA signaling in the fungus-challenged plants. However, the hyperresistance of the JA pathway mutants opr3, coi1, and jar1 indicates that this pathway contributes to susceptibility. Genetic and biochemical experiments indicate that the JA pathway promotes disease by attenuating the activation of SA signaling in fungus-inoculated plants. However, the hypersusceptibility of the jar1 npr1 double mutant compared with the npr1 mutant suggests that JAR1 also contributes to defense, signifying a dichotomous role of JA and a JAR1-dependent mechanism in this interaction.

Effect of salicylic acid on Fusarium graminearum, the major causal agent of fusarium head blight in wheat

2012 ◽  
Vol 116 (3) ◽  
pp. 413-426 ◽  
Author(s):  
Peng-Fei Qi ◽  
Anne Johnston ◽  
Margaret Balcerzak ◽  
Hélène Rocheleau ◽  
Linda J. Harris ◽  
...  
Keyword(s):  
Salicylic Acid ◽  
Fusarium Head Blight ◽  
Fusarium Graminearum ◽  
Causal Agent ◽  
Head Blight

scholarly journals Genomic analysis of host–pathogen interaction between Fusarium graminearum and wheat during early stages of disease development

Microbiology ◽  
2006 ◽  
Vol 152 (6) ◽  
pp. 1877-1890 ◽  
Author(s):  
Rubella S. Goswami ◽  
Jin-Rong Xu ◽  
Frances Trail ◽  
Karen Hilburn ◽  
H. Corby Kistler
Keyword(s):  
Fusarium Graminearum ◽  
Response Regulator ◽  
Gene Prediction ◽  
Genomic Analysis ◽  
Bioinformatic Analysis ◽  
Gene Replacement ◽  
Cdna Libraries ◽  
Disease Development ◽  
Head Blight ◽  
Fungal Genes

Fusarium graminearum strains responsible for causing the plant disease Fusarium head blight vary greatly in their ability to cause disease and produce mycotoxins on wheat. With the goal of understanding fungal gene expression related to pathogenicity, three cDNA libraries were created by suppression subtractive hybridization using wheat heads inoculated with a highly aggressive strain and either water or a less aggressive strain of this pathogen. Eighty-four fungal genes expressed during initial disease development were identified. The probable functions of 49 of these genes could be inferred by bioinformatic analysis. Thirty-five ESTs had no known homologues in current databases and were not identified by ab initio gene prediction methods. These ESTs from infected wheat heads probably represent F. graminearum genes that previously were not annotated. Four genes represented in one of these libraries were selected for targeted gene replacement, leading to the characterization of a two-component response regulator homologue involved in pathogenicity of the fungus. The mutants for this gene showed reduced sporulation and delayed spread of Fusarium head blight on wheat.

scholarly journals PvPGIP2 Accumulation in Specific Floral Tissues But Not in the Endosperm Limits Fusarium graminearum Infection in Wheat

2016 ◽  
Vol 29 (10) ◽  
pp. 815-821 ◽  
Author(s):  
Silvio Tundo ◽  
Michela Janni ◽  
Ilaria Moscetti ◽  
Giulia Mandalà ◽  
Daniel Savatin ◽  
...  
Keyword(s):  
Fusarium Graminearum ◽  
Grain Quality ◽  
Constitutive Expression ◽  
Microbial Pathogens ◽  
Cell Wall Proteins ◽  
Symptom Development ◽  
Head Blight ◽  
Fusarium Spp ◽  
Floral Tissue ◽  
Pathogen Entry

Fusarium head blight (FHB) caused by Fusarium graminearum is one of the most destructive fungal diseases of wheat worldwide. The pathogen infects the spike at flowering time and causes severe yield losses, deterioration of grain quality, and accumulation of mycotoxins. The understanding of the precise means of pathogen entry and colonization of floral tissue is crucial to providing effective protection against FHB. Polygalacturonase (PG) inhibiting proteins (PGIPs) are cell-wall proteins that inhibit the activity of PGs, a class of pectin-depolymerizing enzymes secreted by microbial pathogens, including Fusarium spp. The constitutive expression of a bean PGIP (PvPGIP2) limits FHB symptoms and reduces mycotoxin accumulation in wheat grain. To better understand which spike tissues play major roles in limiting F. graminearum infection, we explored the use of PvPGIP2 to defend specific spike tissues. We show here that the simultaneous expression of PvPGIP2 in lemma, palea, rachis, and anthers reduced FHB symptoms caused by F. graminearum compared with symptoms in infected nontransgenic plants. However, the expression of PvPGIP2 only in the endosperm did not affect FHB symptom development, indicating that once the pathogen has reached the endosperm, inhibition of the pathogen’s PG activity is not effective in preventing its further spread.

scholarly journals Fusarium graminearum FgCWM1 Encodes a Cell Wall Mannoprotein Conferring Sensitivity to Salicylic Acid and Virulence to Wheat

Toxins ◽  
2019 ◽  
Vol 11 (11) ◽  
pp. 628 ◽  
Author(s):  
Ya-Zhou Zhang ◽  
Qing Chen ◽  
Cai-Hong Liu ◽  
Lu Lei ◽  
Yang Li ◽  
...  
Keyword(s):  
Cell Wall ◽  
Salicylic Acid ◽  
Fusarium Graminearum ◽  
Defense Responses ◽  
Protein Accumulation ◽  
Head Blight ◽  
Fungal Cell ◽  
Positive Role ◽  
A Cell

Fusarium graminearum causes Fusarium head blight (FHB), a devastating disease of wheat. Salicylic acid (SA) is involved in the resistance of wheat to F. graminearum. Cell wall mannoprotein (CWM) is known to trigger defense responses in plants, but its role in the pathogenicity of F. graminearum remains unclear. Here, we characterized FgCWM1 (FG05_11315), encoding a CWM in F. graminearum. FgCWM1 was highly expressed in wheat spikes by 24 h after initial inoculation and was upregulated by SA. Disruption of FgCWM1 (ΔFgCWM1) reduced mannose and protein accumulation in the fungal cell wall, especially under SA treatment, and resulted in defective fungal cell walls, leading to increased fungal sensitivity to SA. The positive role of FgCWM1 in mannose and protein accumulation was confirmed by its expression in Saccharomyces cerevisiae. Compared with wild type (WT), ΔFgCWM1 exhibited reduced pathogenicity toward wheat, but it produced the same amount of deoxynivalenol both in culture and in spikes. Complementation of ΔFgCWM1 with FgCWM1 restored the WT phenotype. Localization analyses revealed that FgCWM1 was distributed on the cell wall, consistent with its structural role. Thus, FgCWM1 encodes a CWM protein that plays an important role in the cell wall integrity and pathogenicity of F. graminearum.

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