Summary Sclerotinia sclerotiorum , a predominately necrotrophic fungal pathogen with a broad host range, causes a significant yield‐limiting disease of soybean called Sclerotinia stem rot. Resistance mechanisms against this pathogen in soybean are poorly understood, thus hindering the commercial deployment of resistant varieties. We used a multiomic approach utilizing RNA ‐sequencing, gas chromatography–mass spectrometry‐based metabolomics and chemical genomics in yeast to decipher the molecular mechanisms governing resistance to S. sclerotiorum in soybean. Transcripts and metabolites of two soybean recombinant inbred lines, one resistant and one susceptible to S. sclerotiorum were analysed in a time course experiment. The combined results show that resistance to S. sclerotiorum in soybean is associated in part with an early accumulation of JA ‐Ile ((+)‐7‐iso‐jasmonoyl‐L‐isoleucine), a bioactive jasmonate, increased ability to scavenge reactive oxygen species, and importantly, a reprogramming of the phenylpropanoid pathway leading to increased antifungal activities. Indeed, we noted that phenylpropanoid pathway intermediates, such as 4‐hydroxybenzoate, cinnamic acid, ferulic acid and caffeic acid, were highly accumulated in the resistant line. In vitro assays show that these metabolites and total stem extracts from the resistant line clearly affect S. sclerotiorum growth and development. Using chemical genomics in yeast, we further show that this antifungal activity targets ergosterol biosynthesis in the fungus, by disrupting enzymes involved in lipid and sterol biosynthesis. Overall, our results are consistent with a model where resistance to S. sclerotiorum in soybean coincides with an early recognition of the pathogen, leading to the modulation of the redox capacity of the host and the production of antifungal metabolites.

Background Sclerotinia sclerotiorum is a broad-host range necrotrophic pathogen which is the causative agent of Sclerotinia stem rot (SSR), and a major disease of soybean ( Glycine max ). A time course transcriptomic analysis was performed in both compatible and incompatible soybean lines to identify pathogenicity and developmental factors utilized by S. sclerotiorum to achieve pathogenic success. Results A comparison of genes expressed during early infection identified the potential importance of toxin efflux and nitrogen metabolism during the early stages of disease establishment. The later stages of infection were characterized by an apparent shift to survival structure formation. Analysis of genes highly upregulated in-planta revealed a temporal regulation of hydrolytic and detoxification enzymes, putative secreted effectors, and secondary metabolite synthesis genes. Redox regulation also appears to play a key role during the course of infection, as suggested by the high expression of genes involved in reactive oxygen species production and scavenging. Finally, distinct differences in early gene expression were noted based on the comparison of S. sclerotiorum infection of resistant and susceptible soybean lines. Conclusions Although many potential virulence factors have been noted in the S. sclerotiorum pathosystem, this study serves to highlight soybean specific processes most likely to be critical in successful infection. Functional studies of genes identified in this work are needed to confirm their importance to disease development, and may constitute valuable targets of RNAi approaches to improve resistance to SSR. Electronic supplementary material The online version of this article (10.1186/s12864-019-5517-4) contains supplementary material, which is available to authorized users.

While fungal biotrophs are dependent on successfully suppressing/subverting host defenses during their interaction with live cells, necrotrophs, due to their lifestyle are often confronted with a suite of toxic metabolites. These include an assortment of plant defense compounds (PDCs) which can demonstrate broad antifungal activity. These PDCs can be either constitutively present in plant tissue or induced in response to infection, but are nevertheless an important obstacle which needs to be overcome for successful pathogenesis. Fungal necrotrophs have developed a number of strategies to achieve this goal, from the direct detoxification of these compounds through enzymatic catalysis and modification, to the active transport of various PDCs to achieve toxin sequestration and efflux. Studies have shown across multiple pathogens that the efficient detoxification of host PDCs is both critical for successful infection and often a determinant factor in pathogen host range. Here, we provide a broad and comparative overview of the various mechanisms for PDC detoxification which have been identified in both fungal necrotrophs and fungal pathogens which depend on detoxification during a necrotrophic phase of infection. Furthermore, the effect that these mechanisms have on fungal host range, metabolism, and disease control will be discussed.

A novel virus was detected in grapevines by Illumina sequencing during the screening of two table grape (Vitis vinifera) accessions, cultivars Black Beet and Nagano Purple, from South Korea. The monopartite circular ssDNA genome sequence was subsequently confirmed by rolling cycle amplification, cloning and Sanger sequencing. The complete viral genomic sequence from both accessions ranged from 2,903 to 2,907 nucleotides in length and contained the conserved nonanucleotide sequence TAATATT↓AC and other sequence features typical of the family Geminiviridae, including two predicted sense and four complementary-sense open reading frames. Phylogenetic analysis placed the novel virus in a unique taxon within the family Geminiviridae. A naturally occurring defective subviral DNA was also discovered. This defective DNA molecule carried a deletion of approximately 46% of the full-length genome. Both the genomic and defective DNA molecules were graft-transmissible although no disease is yet correlated with their occurrence in Vitis spp. The tentative names Grapevine geminivirus A (GGVA) and GGVA defective DNA (GGVA D-DNA) are proposed. PCR assays developed using primers designed in the coat protein gene led to the detection of GGVA in 1.74% of 1,262 vines derived from 15 grapevine cultivars from six countries across three continents.

Pistachio (Pistacia vera L.) trees from the National Clonal Germplasm Repository (NCGR) and orchards in California were surveyed for viruses and virus-like agents by high-throughput sequencing (HTS). Analyses of sequence information from 60 trees identified a novel virus, provisionally named “Pistachio ampelovirus A” (PAVA), in the NCGR that showed low amino acid sequence identity (approximately 42%) compared with members of the genus Ampelovirus (family Closteroviridae). A putative viroid, provisionally named “Citrus bark cracking viroid-pistachio” (CBCVd-pis), was also found in the NCGR and showed approximately 87% similarity to Citrus bark cracking viroid (CBCVd, genus Cocadviroid, family Pospiviroidae). Both PAVA and CBCVd-pis were graft transmissible to healthy UCB-1 hybrid rootstock seedlings (P. atlantica × P. integerrima). A field survey of 123 trees from commercial orchards found no incidence of PAVA but five (4%) samples were infected with CBCVd-pis. Of 675 NCGR trees, 16 (2.3%) were positive for PAVA and 172 (25.4%) were positive for CBCVd-pis by reverse-transcription polymerase chain reaction. Additionally, several contigs across multiple samples exhibited significant sequence similarity to a number of other plant virus species in different families. These findings require further study and confirmation. This study establishes the occurrence of viral and viroid populations infecting pistachio trees.