Fusarium crown rot(FCR),predominantly caused by Fusarium pseudograminearum,has been listed as a Category Ⅱ disease in six provinces of China,posing a significant threat to wheat production.The phenylpyrrole fungicide...Fusarium crown rot(FCR),predominantly caused by Fusarium pseudograminearum,has been listed as a Category Ⅱ disease in six provinces of China,posing a significant threat to wheat production.The phenylpyrrole fungicide fludioxonil is a key agent for FCR control.Previous studies indicated that resistance to fludioxonil in F.pseudograminearum is primarily associated with altered expression levels of the FpOS1 gene,which encodes a hybrid histidine kinase.However,the roles of mutations in other FpOS genes and the molecular interactions between FpOS proteins and fludioxonil remain elusive.To address these gaps,we generated 16 fludioxonil-resistant mutants with heritable resistance traits by in vitro selection of four sensitive F.pseudograminearum isolates.These mutants exhibited high resistance levels,with resistance factors(RF)ranging from 633.73 to 8617.07.Compared to their parental isolates,the resistant mutants showed significantly reduced mycelial growth rate,sporulation capacity,and pathogenicity.They were also more sensitive to ionic,osmotic,and oxidative stresses and displayed compromised cell wall and membrane integrity.Fludioxonil demonstrated no cross-resistance with tebuconazole or pydiflumetofen;however,it exhibited weak positive crossresistance to pyraclostrobin and moderate positive cross-resistance to iprodione.Fludioxonil treatment significantly promoted glycerol synthesis and inhibited deoxynivalenol(DON)production in parental isolates,whereas these regulatory effects were markedly attenuated in the resistant mutants.Mutation analysis identified mutation sites in FpOS1,FpOS4,and FpOS5 genes,with a lower mutation frequency in FpOS1 and no mutations detected in FpOS2.Molecular docking indicated that amino acid substitutions in FpOS4 and FpOS5 significantly reduced the binding affinity of fludioxonil to these target proteins.In conclusion,F.pseudograminearum poses a moderate risk of resistance to fludioxonil.Point mutations in FpOS4 and FpOS5 genes emerge as key molecular drivers of resistance,likely by diminishing the binding affinity between the fungicide and its proteins.This study clarifies the molecular basis of fludioxonil resistance in F.pseudograminearum and provides a scientific rationale for the judicious use of this fungicide in managing FCR.展开更多
The predominant causal agent of poplar leaf blight is the pathogenic fungus Alternaria alternata (Fr.) Keissl., which exhibits host specificity toward Populus species. To elucidate the molecular response mechanisms of...The predominant causal agent of poplar leaf blight is the pathogenic fungus Alternaria alternata (Fr.) Keissl., which exhibits host specificity toward Populus species. To elucidate the molecular response mechanisms of A. alternata under fludioxonil fungicide stress, the fungus was cultured at the half-maximal effective concentration (EC₅₀) of fludioxonil. Transcriptomic and metabolomic profiles were analyzed using mycelia harvested under these conditions. Comparative analysis revealed 1,001 differentially expressed genes (DEGs) in the resistant strain (RS) relative to the wild-type strain (WT), comprising 628 upregulated and 373 downregulated genes. Concurrently, 524 differentially accumulated metabolites (DAMs) were identified, with 336 upregulated and 188 downregulated metabolites. KEGG pathway enrichment demonstrated pronounced upregulation in glycerophospholipid metabolism, α-linolenic acid metabolism, nucleic acid biosynthesis, and glycosylation processes. Conversely, arachidonic acid and galactose metabolism pathways were suppressed. Significant downregulation was observed in phosphatidylinositol signaling, aflatoxin biosynthesis, and cutin/suberin/wax biosynthesis pathways. Transcriptomic profiling further indicated that upregulated DEGs were predominantly associated with amino sugar/nucleotide sugar metabolism, ABC transporters, aflatoxin biosynthesis, and purine metabolism, while downregulated DEGs were enriched in N-glycan biosynthesis, endoplasmic reticulum protein processing, steroid biosynthesis, and riboflavin metabolism. Fludioxonil exerted substantial inhibitory effects on fungal growth, pathogenicity, and metabolic activity. Mechanistically, A. alternata counteracted fungicide-induced stress through modulation of its antioxidant defense system. This integrative multi-omics study delineates the dynamic gene expression and metabolic reprogramming in A. alternata under fludioxonil exposure, providing novel insights into potential molecular targets and informing the development of next-generation fungicidal strategies for phytopathogen control.展开更多
Fusarium head blight(FHB)caused by Fusarium graminearum complex is a worldwide devastating disease of wheat,barley,maize,and other cereals.In the field,application of fungicides is one of the main strategies for manag...Fusarium head blight(FHB)caused by Fusarium graminearum complex is a worldwide devastating disease of wheat,barley,maize,and other cereals.In the field,application of fungicides is one of the main strategies for management of FHB.With the long-time usage of fungicides,resistant pathogen populations have become a new challenge for disease management.Application of new pesticide is necessary for sustainable control of this disease.The phenylpyrrole fungicide fludioxonil has been registered recently for management of FHB.However,the resistance mechanisms of F.graminearum to this compound are largely unknown.Here we isolated a biocontrol bacterium Burkholderia pyrrocina W1,which produced the antifungal compound pyrrolnitrin and showed greatly antagonistic activity towards FHB.Spontaneous mutants of pyrrolnitrin-resistant F.graminearum were induced and re-sequenced.Single base mutations were identified in the genes encoding the osmoregulation MAP kinase Hog1 and the AMP dependent kinase Snf1 in pyrrolnitrin-resistant mutants.Snf1 was further confirmed to interact with Hog1 and involved in the response of this fungus to pyrrolnitrin and its derivate,the fungicide fludioxonil.This study reveals that the Snf1 interacts with Hog1 to regulate fludioxonil resistance in a pathogenic fungus.展开更多
[目的]测定噻呋酰胺与咯菌腈防治水稻纹枯病的最佳复配比例。[方法]采用盆栽法评价噻呋酰胺、咯菌腈及各配比对水稻纹枯病的防效,用孙云沛法评价各配比的增效作用。[结果]噻呋酰胺与咯菌腈1:1和1:4时EC50值分别为13.74、13.9 mg/L,CTC...[目的]测定噻呋酰胺与咯菌腈防治水稻纹枯病的最佳复配比例。[方法]采用盆栽法评价噻呋酰胺、咯菌腈及各配比对水稻纹枯病的防效,用孙云沛法评价各配比的增效作用。[结果]噻呋酰胺与咯菌腈1:1和1:4时EC50值分别为13.74、13.9 mg/L,CTC值分别为163.98和187.67,增效明显。综合考虑药效和成本,选择噻呋酰胺与咯菌腈1:1制成25%噻呋酰胺·咯菌腈SC,田间试验表明,在60 g a.i./hm2剂量下对水稻纹枯病的防效为90.6%,优于对照药剂噻呋酰胺和井冈霉素。[结论]噻呋酰胺与咯菌腈混配对水稻纹枯病有优异的防效,值得推广应用。展开更多
基金Supported by Funding from the Henan Provincial Scientific and Technological Breakthrough Project(No.242102111113).
文摘Fusarium crown rot(FCR),predominantly caused by Fusarium pseudograminearum,has been listed as a Category Ⅱ disease in six provinces of China,posing a significant threat to wheat production.The phenylpyrrole fungicide fludioxonil is a key agent for FCR control.Previous studies indicated that resistance to fludioxonil in F.pseudograminearum is primarily associated with altered expression levels of the FpOS1 gene,which encodes a hybrid histidine kinase.However,the roles of mutations in other FpOS genes and the molecular interactions between FpOS proteins and fludioxonil remain elusive.To address these gaps,we generated 16 fludioxonil-resistant mutants with heritable resistance traits by in vitro selection of four sensitive F.pseudograminearum isolates.These mutants exhibited high resistance levels,with resistance factors(RF)ranging from 633.73 to 8617.07.Compared to their parental isolates,the resistant mutants showed significantly reduced mycelial growth rate,sporulation capacity,and pathogenicity.They were also more sensitive to ionic,osmotic,and oxidative stresses and displayed compromised cell wall and membrane integrity.Fludioxonil demonstrated no cross-resistance with tebuconazole or pydiflumetofen;however,it exhibited weak positive crossresistance to pyraclostrobin and moderate positive cross-resistance to iprodione.Fludioxonil treatment significantly promoted glycerol synthesis and inhibited deoxynivalenol(DON)production in parental isolates,whereas these regulatory effects were markedly attenuated in the resistant mutants.Mutation analysis identified mutation sites in FpOS1,FpOS4,and FpOS5 genes,with a lower mutation frequency in FpOS1 and no mutations detected in FpOS2.Molecular docking indicated that amino acid substitutions in FpOS4 and FpOS5 significantly reduced the binding affinity of fludioxonil to these target proteins.In conclusion,F.pseudograminearum poses a moderate risk of resistance to fludioxonil.Point mutations in FpOS4 and FpOS5 genes emerge as key molecular drivers of resistance,likely by diminishing the binding affinity between the fungicide and its proteins.This study clarifies the molecular basis of fludioxonil resistance in F.pseudograminearum and provides a scientific rationale for the judicious use of this fungicide in managing FCR.
基金supported by the Northeast Asia Biodiversity Research Center(grant number 411147021003).
文摘The predominant causal agent of poplar leaf blight is the pathogenic fungus Alternaria alternata (Fr.) Keissl., which exhibits host specificity toward Populus species. To elucidate the molecular response mechanisms of A. alternata under fludioxonil fungicide stress, the fungus was cultured at the half-maximal effective concentration (EC₅₀) of fludioxonil. Transcriptomic and metabolomic profiles were analyzed using mycelia harvested under these conditions. Comparative analysis revealed 1,001 differentially expressed genes (DEGs) in the resistant strain (RS) relative to the wild-type strain (WT), comprising 628 upregulated and 373 downregulated genes. Concurrently, 524 differentially accumulated metabolites (DAMs) were identified, with 336 upregulated and 188 downregulated metabolites. KEGG pathway enrichment demonstrated pronounced upregulation in glycerophospholipid metabolism, α-linolenic acid metabolism, nucleic acid biosynthesis, and glycosylation processes. Conversely, arachidonic acid and galactose metabolism pathways were suppressed. Significant downregulation was observed in phosphatidylinositol signaling, aflatoxin biosynthesis, and cutin/suberin/wax biosynthesis pathways. Transcriptomic profiling further indicated that upregulated DEGs were predominantly associated with amino sugar/nucleotide sugar metabolism, ABC transporters, aflatoxin biosynthesis, and purine metabolism, while downregulated DEGs were enriched in N-glycan biosynthesis, endoplasmic reticulum protein processing, steroid biosynthesis, and riboflavin metabolism. Fludioxonil exerted substantial inhibitory effects on fungal growth, pathogenicity, and metabolic activity. Mechanistically, A. alternata counteracted fungicide-induced stress through modulation of its antioxidant defense system. This integrative multi-omics study delineates the dynamic gene expression and metabolic reprogramming in A. alternata under fludioxonil exposure, providing novel insights into potential molecular targets and informing the development of next-generation fungicidal strategies for phytopathogen control.
基金supported by the National Natural Science Foundation of China(32102241,U21A20219)China Postdoctoral Science Foundation(2021M702882)China Agriculture Research System(CARS-03–29).
文摘Fusarium head blight(FHB)caused by Fusarium graminearum complex is a worldwide devastating disease of wheat,barley,maize,and other cereals.In the field,application of fungicides is one of the main strategies for management of FHB.With the long-time usage of fungicides,resistant pathogen populations have become a new challenge for disease management.Application of new pesticide is necessary for sustainable control of this disease.The phenylpyrrole fungicide fludioxonil has been registered recently for management of FHB.However,the resistance mechanisms of F.graminearum to this compound are largely unknown.Here we isolated a biocontrol bacterium Burkholderia pyrrocina W1,which produced the antifungal compound pyrrolnitrin and showed greatly antagonistic activity towards FHB.Spontaneous mutants of pyrrolnitrin-resistant F.graminearum were induced and re-sequenced.Single base mutations were identified in the genes encoding the osmoregulation MAP kinase Hog1 and the AMP dependent kinase Snf1 in pyrrolnitrin-resistant mutants.Snf1 was further confirmed to interact with Hog1 and involved in the response of this fungus to pyrrolnitrin and its derivate,the fungicide fludioxonil.This study reveals that the Snf1 interacts with Hog1 to regulate fludioxonil resistance in a pathogenic fungus.
文摘[目的]测定噻呋酰胺与咯菌腈防治水稻纹枯病的最佳复配比例。[方法]采用盆栽法评价噻呋酰胺、咯菌腈及各配比对水稻纹枯病的防效,用孙云沛法评价各配比的增效作用。[结果]噻呋酰胺与咯菌腈1:1和1:4时EC50值分别为13.74、13.9 mg/L,CTC值分别为163.98和187.67,增效明显。综合考虑药效和成本,选择噻呋酰胺与咯菌腈1:1制成25%噻呋酰胺·咯菌腈SC,田间试验表明,在60 g a.i./hm2剂量下对水稻纹枯病的防效为90.6%,优于对照药剂噻呋酰胺和井冈霉素。[结论]噻呋酰胺与咯菌腈混配对水稻纹枯病有优异的防效,值得推广应用。
