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In 2017–2018, extensive symptoms of sudden decline and fruit rot were observed on date palms in southern Tunisia. Samples of diseased plants were randomly collected in six localities. Based on morphological identification, Fusarium was the most frequent fungal genus detected. A sequencing of translation elongation factor, calmodulin, and second largest subunit of RNA polymerase II genes was used to identify 63 representative Fusarium strains at species level and investigate their phylogenetic relationships. The main species detected was Fusarium proliferatum, and at a much lesser extent, Fusarium brachygibbosum, Fusarium caatingaense, Fusarium clavum, Fusarium incarnatum, and Fusarium solani. Pathogenicity on the Deglet Nour variety plantlets and the capability to produce mycotoxins were also assessed. All Fusarium species were pathogenic complying Koch’s postulates. Fusarium proliferatum strains produced mainly fumonisins (FBs), beauvericin (BEA), and, to a lesser extent, enniatins (ENNs) and moniliformin (MON). All F. brachygibbosum strains produced low levels of BEA, diacetoxyscirpenol, and neosolaniol; two strains produced also T-2 toxin, and a single strain produced HT-2 toxin. Fusarium caatingaense, F. clavum, F. incarnatum produced only BEA. Fusarium solani strains produced MON, BEA, and ENNs. This work reports for the first time a comprehensive multidisciplinary study of Fusarium species on date palms, concerning both phytopathological and food safety issues.

Fusarium head blight (FHB) is a devastating disease occurring in small grain cereals worldwide. The disease results in the reduction of grain yield, and mycotoxins accumulated in grain are also harmful to both humans and animals. It has been reported that response to pathogen infection may be associated with the morphological and developmental traits of the host plant, e.g. earliness and plant height. Despite many studies, effective markers for selection of barley genotypes with increased resistance to FHB have not been developed. In the present study, we investigated 100 recombinant inbred lines (RIL) of spring barley. Plants were examined in field conditions (three locations) in a completely randomized design with three replications. Barley genotypes were artificially infected with spores of Fusarium culmorum before heading. Apart from the main phenotypic traits (plant height, spike characteristic, grain yield), infected kernels were visually scored and the content of deoxynivalenol (DON) mycotoxin was investigated. A set of 70 Quantitative Trait Loci (QTLs) were detected through phenotyping of the mapping population in field conditions and genotyping using a barley Ilumina 9K iSelect platform. Six loci were detected for the FHB index on chromosomes 2H, 3H, 5H, and 7H. A region on the short arm of chromosome 2H was detected in which many QTLs associated with FHB- and yield-related traits were found. This study confirms that agromorphological traits are tightly related to FHB and should be taken into consideration when breeding barley plants for FHB resistance.

Fusarium species are among the most important phytopathogenic and toxigenic fungi. To understand the molecular underpinnings of pathogenicity in the genus Fusarium, we compared the genomes of three phenotypically diverse species: Fusarium graminearum, Fusarium verticillioides and Fusarium oxysporum f. sp. lycopersici. Our analysis revealed lineage-specific (LS) genomic regions in F. oxysporum that include four entire chromosomes and account for more than one-quarter of the genome. LS regions are rich in transposons and genes with distinct evolutionary profiles but related to pathogenicity, indicative of horizontal acquisition. Experimentally, we demonstrate the transfer of two LS chromosomes between strains of F. oxysporum, converting a non-pathogenic strain into a pathogen. Transfer of LS chromosomes between otherwise genetically isolated strains explains the polyphyletic origin of host specificity and the emergence of new pathogenic lineages in F. oxysporum. These findings put the evolution of fungal pathogenicity into a new perspective

Fusarium diseases of small grain cereals and maize cause significant yield losses worldwide. Fusarium infections result in reduced grain yield and contamination with mycotoxins, some of which have a notable impact on human and animal health. Regulations on maximum limits have been established in various countries to protect consumers from the harmful effects of these mycotoxins. Several factors are involved in Fusarium disease and mycotoxin occurrence and among them environmental factors and the agronomic practices have been shown to deeply affect mycotoxin contamination in the field. In the present review particular emphasis will be placed on how environmental conditions and stress factors for the crops can affect Fusarium infection and mycotoxin production, with the aim to provide useful knowledge to develop strategies to prevent mycotoxin accumulation in cereals.

Fusarium graminearum is a causal agent of Fusarium head blight (FHB) and a deoxynivalenol (DON) producer. In this study, OSP24 is identified as an important virulence factor in systematic characterization of the 50 orphan secreted protein ( OSP ) genes of F. graminearum . Although dispensable for growth and initial penetration, OSP24 is important for infectious growth in wheat rachis tissues. OSP24 is specifically expressed during pathogenesis and its transient expression suppresses BAX- or INF1-induced cell death. Osp24 is translocated into plant cells and two of its 8 cysteine-residues are required for its function. Wheat SNF1-related kinase TaSnRK1α is identified as an Osp24-interacting protein and shows to be important for FHB resistance in TaSnRK1α-overexpressing or silencing transgenic plants. Osp24 accelerates the degradation of TaSnRK1α by facilitating its association with the ubiquitin-26S proteasome. Interestingly, TaSnRK1α also interacts with TaFROG, an orphan wheat protein induced by DON. TaFROG competes against Osp24 for binding with the same region of TaSnRKα and protects it from degradation. Overexpression of TaFROG stabilizes TaSnRK1α and increases FHB resistance. Taken together, Osp24 functions as a cytoplasmic effector by competing against TaFROG for binding with TaSnRK1α, demonstrating the counteracting roles of orphan proteins of both host and fungal pathogens during their interactions. Fusarium graminearum is a major fungal pathogen of cereals. Here the authors show that F. graminearum secretes an effector, Osp24, that induces degradation of the wheat TaSnRK1α kinase to promote disease while an orphan wheat protein, TaFROG1, can compete with Osp24 for binding to TaSnRK1α and protect it from degradation

Plant genomes encode hundreds of receptor kinases and peptides, but the number of known plant receptor-ligand pairs is limited. We report that the Arabidopsis leucine-rich repeat receptor kinase LRR-RK MALE DISCOVERER 1-INTERACTING RECEPTOR LIKE KINASE 2 (MIK2) is the receptor for the SERINE RICH ENDOGENOUS PEPTIDE (SCOOP) phytocytokines. MIK2 is necessary and sufficient for immune responses triggered by multiple SCOOP peptides, suggesting that MIK2 is the receptor for this divergent family of peptides. Accordingly, the SCOOP12 peptide directly binds MIK2 and triggers complex formation between MIK2 and the BRASSINOSTEROID INSENSITIVE 1-ASSOCIATED KINASE 1 (BAK1) co-receptor. MIK2 is required for resistance to the important root pathogen Fusarium oxysporum . Notably, we reveal that Fusarium proteomes encode SCOOP-like sequences, and corresponding synthetic peptides induce MIK2-dependent immune responses. These results suggest that MIK2 may recognise Fusarium -derived SCOOP-like sequences to induce immunity against Fusarium . The definition of SCOOPs as MIK2 ligands will help to unravel the multiple roles played by MIK2 during plant growth, development and stress responses. Secreted peptides and cell-surface localized receptor kinases allow plants to modify growth and development according to external cues. Here, Rhodes et al. show that the MIK2 receptor perceives the SERINE RICH ENDOGENOUS PEPTIDE (SCOOP) family of phytocytokines and is capable of recognising Fusarium -derived SCOOP-like peptides.

Interactions between bacteria and fungi have great environmental, medical, and agricultural importance, but the molecular mechanisms are largely unknown. Here, we study the interactions between the bacterium Pseudomonas piscium , from the wheat head microbiome, and the plant pathogenic fungus Fusarium graminearum . We show that a compound secreted by the bacteria (phenazine-1-carboxamide) directly affects the activity of fungal protein FgGcn5, a histone acetyltransferase of the SAGA complex. This leads to deregulation of histone acetylation at H2BK11, H3K14, H3K18, and H3K27 in F . graminearum , as well as suppression of fungal growth, virulence, and mycotoxin biosynthesis. Therefore, an antagonistic bacterium can inhibit growth and virulence of a plant pathogenic fungus by manipulating fungal histone modification. The molecular mechanisms behind the interactions between bacteria and fungi are largely unclear. Here, Chen et al. show that a compound secreted by bacteria from the wheat head microbiome inhibits growth and virulence of a plant pathogenic fungus by manipulating fungal histone modification.

Fusarium graminearum is a destructive wheat pathogen. No fully resistant cultivars are available. Knowledge concerning the molecular weapons of F. graminearum to achieve infection remains limited. Here, we report that deletion of the putative secondary metabolite biosynthesis gene cluster fg3_54 compromises the pathogen’s ability to infect wheat through cell-to-cell penetration. Ectopic expression of fgm4 , a pathway-specific bANK-like regulatory gene, activates the transcription of the fg3_54 cluster in vitro. We identify a linear, C- terminally reduced and d -amino acid residue-rich octapeptide, fusaoctaxin A, as the product of the two nonribosomal peptide synthetases encoded by fg3_54 . Chemically-synthesized fusaoctaxin A restores cell-to-cell invasiveness in fg3_54 -deleted F. graminearum , and enables colonization of wheat coleoptiles by two Fusarium strains that lack the fg3_54 homolog and are nonpathogenic to wheat. In conclusion, our results identify fusaoctaxin A as a virulence factor required for cell-to-cell invasion of wheat by F. graminearum . Fusarium graminearum is a fungal pathogen of wheat and other cereals. Here the authors identify a gene cluster in F. graminearum encoding the production of a non-ribosomal peptide that is required for infection of wheat through cell-to-cell penetration.

Banana ( Musa spp.) is a staple food for more than 400 million people. Over 40% of world production and virtually all the export trade is based on Cavendish banana. However, Cavendish banana is under threat from a virulent fungus, Fusarium oxysporum f. sp. cubense tropical race 4 (TR4) for which no acceptable resistant replacement has been identified. Here we report the identification of transgenic Cavendish with resistance to TR4. In our 3-year field trial, two lines of transgenic Cavendish, one transformed with RGA2 , a gene isolated from a TR4-resistant diploid banana, and the other with a nematode-derived gene, Ced9 , remain disease free. Transgene expression in the RGA2 lines is strongly correlated with resistance. Endogenous RGA2 homologs are also present in Cavendish but are expressed tenfold lower than that in our most resistant transgenic line. The expression of these homologs can potentially be elevated through gene editing, to provide non-transgenic resistance. The newly recognized Fusarium wilt pathogen tropical race 4 is threatening worldwide banana production. Here, the authors transform Cavendish bananas with a resistance gene, RGA2 , from diploid banana or a nematode-derived gene, Ced9 , and confer resistance to natural infection under field conditions.

The plant health status is determined by the interplay of plant-pathogen-microbiota in the rhizosphere. Here, we investigate this tripartite system focusing on the pathogen Fusarium oxysporum f. sp. lycopersici (FOL) and tomato plants as a model system. First, we explore differences in tomato genotype resistance to FOL potentially associated with the differential recruitment of plant-protective rhizosphere taxa. Second, we show the production of fusaric acid by FOL to trigger systemic changes in the rhizosphere microbiota. Specifically, we show this molecule to have opposite effects on the recruitment of rhizosphere disease-suppressive taxa in the resistant and susceptible genotypes. Last, we elucidate that FOL and fusaric acid induce changes in the tomato root exudation with direct effects on the recruitment of specific disease-suppressive taxa. Our study unravels a mechanism mediating plant rhizosphere assembly and disease suppression by integrating plant physiological responses to microbial-mediated mechanisms in the rhizosphere. The phytotoxin fusaric acid produced by the phytopathogen Fusarium oxysporum f. sp. lycopersici results in a differential assembly of the rhizosphere microbiota of resistant and susceptible genotypes with implication for disease suppression.