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Development of resistant crops is the most effective way to control plant diseases to safeguard food and feed production. Disease resistance is commonly based on resistance genes, which generally mediate the recognition of small proteins secreted by invading pathogens. These proteins secreted by pathogens are called ‘avirulence’ proteins. Their identification is important for being able to assess the usefulness and durability of resistance genes in agricultural settings. We have used genome sequencing of a set of strains of the melon wilt fungus Fusarium oxysporum f. sp. melonis (Fom), bioinformatics-based genome comparison and genetic transformation of the fungus to identify AVRFOM2, the gene that encodes the avirulence protein recognized by the melon Fom-2 gene. Both an unbiased and a candidate gene approach identified a single candidate for the AVRFOM2 gene. Genetic complementation of AVRFOM2 in three different race 2 isolates resulted in resistance of Fom-2-harbouring melon cultivars. AvrFom2 is a small, secreted protein with two cysteine residues and weak similarity to secreted proteins of other fungi. The identification of AVRFOM2 will not only be helpful to select melon cultivars to avoid melon Fusarium wilt, but also to monitor how quickly a Fom population can adapt to deployment of Fom-2-containing cultivars in the field.

Fusarium oxysporum f. sp. radicis‐cucumerinum (Forc) causes severe root rot and wilt in several cucurbit species, including cucumber, melon, and watermelon. Previously, a pathogenicity chromosome, chrRC, was identified in Forc. Strains that were previously nonpathogenic could infect multiple cucurbit species after obtaining this chromosome via horizontal chromosome transfer (HCT). In contrast, F. oxysporum f. sp. melonis (Fom) can only cause disease on melon plants, even though Fom contains contigs that are largely syntenic with chrRC. The aim of this study was to identify the genetic basis underlying the difference in host range between Fom and Forc. First, colonization of different cucurbit species between Forc and Fom strains showed that although Fom did not reach the upper part of cucumber or watermelon plants, it did enter the root xylem. Second, to select candidate genomic regions associated with differences in host range, high‐quality genome assemblies of Fom001, Fom005, and Forc016 were compared. One of the Fom contigs that is largely syntenic and highly similar in sequence to chrRC contains the effector gene SIX6. After HCT of the SIX6‐containing chromosome from Fom strains to a nonpathogenic strain, the recipient (HCT) strains caused disease on melon plants, but not on cucumber or watermelon plants. These results provide strong evidence that the differences in host range between Fom and Forc are caused by differences between transferred chromosomes of Fom and chrRC, thus narrowing down the search for genes allowing or preventing infection of cucumber and watermelon to genes located on these chromosomes. A mobile pathogenicity chromosome was identified in Fusarium oxysporum that confers pathogenicity towards melon, and this chromosome is highly similar to the chromosome that confers pathogenicity towards multiple cucurbits.

Fusarium oxysoporum f. sp. radicis‐cucumerinum (Forc) is able to cause disease in cucumber, melon, and watermelon, while F. oxysporum f. sp. melonis (Fom) can only infect melon plants. Earlier research showed that mobile chromosomes in Forc and Fom determine the difference in host range between Forc and Fom. By closely comparing these pathogenicity chromosomes combined with RNA‐sequencing data, we selected 11 candidate genes that we tested for involvement in the difference in host range between Forc and Fom. One of these candidates is a putative effector gene on the Fom pathogenicity chromosome that has nonidentical homologs on the Forc pathogenicity chromosome. Four independent Forc transformants with this gene from Fom showed strongly reduced or no pathogenicity towards cucumber, while retaining pathogenicity towards melon and watermelon. This suggests that the protein encoded by this gene is recognized by an immune receptor in cucumber plants. This is the first time that a single gene has been demonstrated to determine a difference in host specificity between formae speciales of F. oxysporum. A single putative effector gene from melon‐infecting Fusarium oxysporum f. sp. melonis is able to turn cucumber‐, melon‐ and watermelon‐infecting F. oxysoporum f. sp. radicis‐cucumerinum nonpathogenic towards cucumber plants.

Watermelon and melon crops are affected by some important soil-borne fungal diseases like carbonaceous rot (Macrophomina phaseolina), collapse (Monosporascus cannonballus), or the most important pathology at an economic level, the Fusarium wilt (Fusarium oxysporum f. sp. niveum, F. oxysporum f. sp. melonis, F. solani f. sp. cucurbitae, Neocosmospora falciformis, and N. keratoplastica). The methods commonly used for their control are often ineffective, thus new approaches, as the use of biological control agents, are constantly being sought. This work aimed to isolate, identify, and test endophytic fungi for their antagonistic properties against the three mentioned diseases. For this, about 350 endophytic fungal strains were isolated from asymptomatic watermelon plants. Among these, 7 fungal species were selected to evaluate their antagonistic potential against 14 pathogens. Dual culture assays allowed to select two Trichoderma strains according to the high inhibition rates observed (up to 93%), that were further employed in melon and watermelon plants, showing that some of the pathogens were controlled in terms of disease incidence, exhibiting a decrease up to 67% for T. lentiforme. In addition, three concentrations of Epicoccum purpurascens extract was selected to evaluate the germicide effect, obtaining significant differences in the growth of the pathogens depending on fermentation parameters.

Fusarium wilt is one of the most destructive and less controllable diseases in melon, which is usually caused by fusarium oxysporum . In this study, transcriptome sequencing and Yeast Two-Hybrid (Y2H) methods were used for quantification of differentially expressed genes (DEGs) involved in fusarium oxysporum (f. sp. melonis race 1) stress-induced mechanisms in contrasted melon varieties (M4-45 “susceptible” and MR-1 “resistant”). The interaction factors of Fom-2 resistance genes were also explored in response to the plant-pathogen infection mechanism. Transcriptomic analysis exhibited total 1,904 new genes; however, candidate DEGs analysis revealed a total of 144 specific genes (50 upregulated and 94 downregulated) for M4-45 variety and 104 specific genes (71 upregulated and 33 downregulated) for MR-1 variety, respectively. The analysis of Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway depicted some candidate DEGs, including Phenylalanine metabolism, phenylpropane biosynthesis, plants-pathogen interaction, and signal transduction of plant hormones, which were mainly involved in disease resistance metabolic pathways. The weighted gene co-expression network analysis (WGCNA) analysis revealed a strong correlation module and exhibited the disease resistance-related genes encoding course proteins, transcription factors, protein kinase, benzene propane biosynthesis path, plants-pathogen interaction pathway, and glutathione S-transferase. Meanwhile, the resistance-related specific genes expression was relatively abundant in MR-1 compared to the M4-45, and cell wall-associated receptor kinases ( MELO3C008452 and MELO3C008453 ), heat shock protein (Cucumis_melo_newGene_172), defensin-like protein (Cucumis_melo_newGene_5490), and disease resistance response protein ( MELO3C016325 ), activator response protein ( MELO3C021623 ), leucine-rich repeat receptor protein kinase ( MELO3C024412 ), lactyl glutathione ligase (Cucumis_melo_newGene_36), and unknown protein ( MELO3C007588 ) were persisted by exhibiting the upregulated expressions. At the transcription level, the interaction factors between the candidate genes in response to the fusarium oxysporum induced stress, and Y2H screening signified the main contribution of MYB transcription factors ( MELO3C009678 and MELO3C014597 ), BZIP ( MELO3C011839 and MELO3C019349 ), unknown proteins, and key enzymes in the ubiquitination process ( 4XM334FK014 ). The candidate genes were further verified in exogenously treated melon plants with f. oxysporum ( Fom-2 , Race 1), Abscisic acid (ABA), Methyl Jasmonite (MeJA), and Salicylic acid (SA), using the fluorescence quantitative polymerase chain reaction (qRT-PCR) analysis. The overall expression results indicated that the SA signal pathway is involved in effective regulation of the Fom-2 gene activity.

The oases environment is favourable for the development of several diseases and the proliferation of insects that transmit viruses. The selection and breeding of local cultivars of cucurbits for resistance to these biotic constraints is the most economic control strategy. Thus the evaluation of resistance of local melon, watermelon and squash cultivars (cv.) to seven viruses (CMV, ZYMV, WMV, PRSV, MWMV, MNSV and TolCNDV) and two fungal pathogens Fusarium oxysporum f. sp. melonis (FOM, races 1 and 2) and Podosphaera xanthii (race 1 (strain Sm3), race 2 (strain S87-7), race 3 (strain 00SM39), race 5 (strain 98Sm65) and race 3–5 (strain 04Sm2)) was made. The results showed that 26 out of 44 cultivars evaluated, exhibited resistance for at least for one of the studied pathogens. The local cucurbit cultivars were generally resistant to MNSV and ToLCNDV in comparison to commercial cultivars. Specifically, melon cultivars M5 and M18, and squash cv. C46, C60 and C65 were resistant to WMV. Watermelon cultivars P15 and P24 along with squash cultivar C60 exhibited resistance to CMV. Partial resistance to MWMV was observed in melon cultivars M35 and M129, watermelon cultivars P35 and P55, and squash cultivar C65. Only C65 squash cv. was resistant to PRSV. For fungal pathogens, the local melon cultivars M6, M26, M58, M120, M131 were resistant to race 1 of FOM, and all studied cultivars were susceptible to race 2 of this fungus. Two local melon cultivars M120 and M122 were resistant to P. xanthii races 1, 2 and 3. The wild desert bitter watermelon was resistant to WMV, MNSV, CMV, MWMV and ToLCNDV, but not to PRSV. This study demonstrated that the Tunisian cucurbit genetic resources present valuable material for improving resistance to viral and fungal diseases in these crops.

A novel mitovirus was identified in Fusarium oxysporum f. sp. melonis strain T-SD3 and designated as \"Fusarium oxysporum mitovirus 3\" (FoMV3). The virus was isolated from diseased muskmelon plants with the typical symptom of fusarium wilt. The complete genome of FoMV3 is 2269 nt in length with a predicted AU content of 61.40% and contains a single open reading frame (ORF) using the fungal mitochondrial genetic code. The ORF was predicted to encode a polypeptide of 679 amino acids (aa) containing a conserved RNA-dependent RNA polymerase (RdRp) domain with a molecular mass of 77.39 kDa, which contains six conserved motifs with the highly conserved GDD tripeptide in motif IV. The 5′-untranslated region (UTR) and 3′-UTR of FoMV3 were predicted to fold into stem-loop structures. BLASTp analysis revealed that the RdRp of FoMV3 shared the highest aa sequence identity (83.85%) with that of Fusarium asiaticum mitovirus 5 (FaMV5, a member of the family Mitoviridae) infecting F. asiaticum, the causal agent of wheat fusarium head blight. Phylogenetic analysis further suggested that FoMV3 is a new member of the genus Unuamitovirus within the family Mitoviridae. This is the first report of a new mitovirus associated with F. oxysporum f. sp. melonis.

Melon Fusarium wilt (MFW), which is caused by Fusarium oxysporum f. sp. melonis (FOM), is a soil-borne disease that commonly impacts melon cultivation worldwide. In the absence of any disease-resistant melon cultivars, the control of MFW relies heavily on the application of chemical fungicides. Fludioxonil, a phenylpyrrole fungicide, has been shown to have broad-spectrum activity against many crop pathogens. Sensitivity analysis experiments suggest that fludioxonil has a strong inhibitory effect on the mycelial growth of FOM isolates. Five fludioxonil-resistant FOM mutants were successfully generated by repeated exposure to fludioxonil under laboratory conditions. Although the mutants exhibited significantly reduced mycelial growth in the presence of the fungicide, there initially appeared to be little fitness cost, with no significant difference (p < 0.05) in the growth rates of the mutants and wild-type isolates. However, further investigation revealed that the sporulation of the fludioxonil-resistant mutants was affected, and mutants exhibited significantly (p < 0.05) reduced growth rates in response to KCl, NaCl, glucose, and mannitol. Meanwhile, molecular analysis of the mutants strongly suggested that the observed fludioxonil resistance was related to changes in the sequence and expression of the FoOs1 gene. In addition, the current study found no evidence of cross-resistance between fludioxonil and any of the other fungicides tested. These results indicate that fludioxonil has great potential as an alternative method of control for FOM in melon crops.

Objective Wilt caused by Fusarium oxysporum f. sp. melonis (Fom) is one of the most widespread and destructive melon diseases worldwide. Whole-genome sequencing data of a diverse set of Fom strains, as well as several non-pathogenic strains isolated from melon from different parts of the world are described here. These data shed light on the genetic diversity, population structure and the potential evolutionary trajectories which have led to the emergence of different Fom races, and will facilitate identification of avirulence genes which will be helpful to develop resistant melon cultivars. Data description Genomic DNA was extracted from mycelium of 38 Fusarium oxysporum (Fo) strains collected from different parts of the world including Belgium, China, France, Iran, Israel, Japan, Mexico, New Zealand, Spain, the Netherlands, and the United States. The genomes were sequenced to ≈ 20 × coverage using the Illumina Hiseq Xten system, resulting in paired-end reads of 151 bp and assemblies of 1675 (Fom-18L) to 4472 (Fom-R12-13) scaffolds. The genome sequences are available in the National Center for Biotechnology Information (NCBI) and the Sequence Read Archive (SRA) under Project number PRJNA596396 and PRJNA596396, respectively. The presented data set can be useful to identify the genes associated with pathogenic strategies.

In the current study, a novel strain of Fusarium oxysporum alternavirus 1 (FoAV1) was identified from the Fusarium oxysporum f. sp. melonis (FOM) strain T-BJ17 and was designated as Fusarium oxysporum alternavirus 1-FOM (FoAV1-FOM). Its genome consists of four dsRNA segments of 3515 bp (dsRNA1), 2663 bp (dsRNA2), 2368 bp (dsRNA3), and 1776 bp (dsRNA4) in length. Open reading frame 1 (ORF1) in dsRNA1 was found to encode a putative RNA-dependent RNA polymerase (RdRp), whose amino acid sequence was 99.02% identical to that of its counterpart in FoAV1; while ORF2 in dsRNA2, ORF3 in dsRNA3, and ORF4 in dsRNA4 were all found to encode hypothetical proteins. Strain T-BJ17-VF, which was verified to FoAV1-FOM-free, was obtained using single-hyphal-tip culture combined with high-temperature treatment to eliminate FoAV1-FOM from strain T-BJ17. The colony growth rate, ability to produce spores, and virulence of strain T-BJ17 were significantly lower than those of T-BJ17-VF, while the dry weight of the mycelial biomass and the sensitivity to difenoconazole and pydiflumetofen of strain T-BJ17 were greater than those of T-BJ17-VF. FoAV1-FOM was capable of 100% vertical transmission via spores. To our knowledge, this is the first time that an alternavirus has infected FOM, and this is the first report of hypovirulence and increased sensitivity to difenoconazole and pydiflumetofen induced by FoAV1-FOM infection in FOM.