Fusarium fujikuroi causes bakanae (“foolish seedling”) disease of rice which is characterized by hyper-elongation of seedlings resulting from production of gibberellic acids (GAs) by the fungus. This plant pathogen is also known for production of harmful mycotoxins, such as fusarins, fusaric acid, apicidin F and beauvericin. Recently, we generated the first de novo genome sequence of F. fujikuroi strain IMI 58289 combined with extensive transcriptional, epigenetic, proteomic and chemical product analyses. GA production was shown to provide a selective advantage during infection of the preferred host plant rice. Here, we provide genome sequences of eight additional F. fujikuroi isolates from distant geographic regions. The isolates differ in the size of chromosomes, most likely due to variability of subtelomeric regions, the type of asexual spores (microconidia and/or macroconidia), and the number and expression of secondary metabolite gene clusters. Whilst most of the isolates caused the typical bakanae symptoms, one isolate, B14, caused stunting and early withering of infected seedlings. In contrast to the other isolates, B14 produced no GAs but high amounts of fumonisins during infection on rice. Furthermore, it differed from the other isolates by the presence of three additional polyketide synthase (PKS) genes (PKS40, PKS43, PKS51) and the absence of the F. fujikuroi-specific apicidin F (NRPS31) gene cluster. Analysis of additional field isolates confirmed the strong correlation between the pathotype (bakanae or stunting/withering), and the ability to produce either GAs or fumonisins. Deletion of the fumonisin and fusaric acid-specific PKS genes in B14 reduced the stunting/withering symptoms, whereas deletion of the PKS51 gene resulted in elevated symptom development. Phylogenetic analyses revealed two subclades of F. fujikuroi strains according to their pathotype and secondary metabolite profiles.
During 2011, Fusarium rot of stored garlic was detected on bulbs of ‘Aglio Bianco’ (white garlic) in Piacenza, Ferrara and Rovigo districts. Bulbs, harvested in July, were asymptomatic. During conservation in the drying sheds, approximately thirty percent of bulbs appeared emptied and softened. Fusarium proliferatum was consistently recovered from infected bulbs. The morphological identification was confirmed by Translation Elongation Factor 1‐alpha gene sequencing. Koch postulates were checked through pathogenicity tests. The disease has already been reported in Serbia, Germany, Spain, United States, China and India, but to our knowledge, this is the first report of F. proliferatum garlic bulb rot in Italy.
Chemotype composition of Fusarium graminearum strains, isolated from durum wheat kernels from naturally FHB infected fields in Northern and Central Italy, was investigated by multiplex PCR. The different climatic and environmental conditions of the two examined areas separated by the Apennines affected the composition of chemotypes. 15Ac-DON chemotype was predominant in both the sub areas. Nivalneol chemotype was more frequent in the warmer sub area.
Root and crown rot of wheat, caused by Fusarium culmorum (Fc), is a serious disease worldwide, particularly in Iran. Currently, the mechanisms underlying resistance to Fusarium-caused diseases are still unknown. Methyl jasmonate (MeJA) has been identified as a vital cellular regulator, and the effect of exogenous MeJA application during wheat-Fc interaction has not been studied previously at the molecular level. This study, using realtime quantitative PCR, was carried out to determine the expression of seven host defense-associated genes consisting of PR3, PR4, PR5, TaPERO, LOX, PAL and cytochrome P450 gene (CYP709C1) at 48, 72 and 96 h after Fc-inoculation (hai) and to investigate the relationship between the induced resistance by MeJA application and the gene expression patterns. The results showed that several genes were induced earlier (48 hai) and to higher levels in the resistant cv. Sumai3 than in susceptible cv. Falat. Many Fc-induced genes were also activated and induced by MeJA particularly during the later stages of infection; however, in contrast to defense-gene induction by the pathogen, there was not a general trend of higher induction in Sumai3 compared to Falat following this chemical treatment. The chemically induced protection significantly reduced the development of necrotic symptoms in both cultivars over a 3-week period after inoculation; however, this reduction was greater in Falat than in Sumai3 relative to the controls. Surprisingly, the expression of these genes was also expressed in crown tissue that had not yet been in contact with the fungus, signifying that a form of systemic response was taking place in this interaction. This is the first work reporting the effect of timing application of MeJA during Fc infection and comparing the defense-related gene expression between root and crown tissues of wheat genotypes. Moreover, soildrench application of MeJA resulted in strong induction, verifying the success of this application method in systemically activating JA signaling for the first time. These results provided important intimations for designing strategies to curtail diseases caused by Fusarium.
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