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Given the increasing demand for wheat which is forecast, cropping of wheat in short rotations will likely remain a common practice. However, in temperate wheat growing regions the soil-borne fungal pathogen Gaeumannomyces tritici becomes a major constraint on productivity. In cultivar rotation field experiments on the Rothamsted Farm (Hertfordshire, UK) we demonstrated a substantial reduction in take-all disease and grain yield increases of up to 2.4 tonnes/ha when a low take-all inoculum building wheat cultivar was grown in the first year of wheat cropping. Phenotyping of 71 modern elite wheat cultivars for the take-all inoculum build-up trait across six diverse trial sites identified a few cultivars which exhibited a consistent lowering of take-all inoculum build-up. However, there was also evidence of a significant interaction effect between trial site and cultivar when a pooled Residual Maximum Likelihood (REML) procedure was conducted. There was no evidence of an unusual rooting phenotype associated with take-all inoculum build-up in two independent field experiments and a sand column experiment. Together our results highlight the complex interactions between wheat genotype, environmental conditions and take-all inoculum build-up. Further work is required to determine the underlying genetic and mechanistic basis of this important phenomenon.

Plants are constantly being challenged by aspiring pathogens, but disease is rare. Why? Broadly, there are three reasons for pathogen failure. Either (1) the plant is unable to support the niche requirements of a potential pathogen and is thus a non-host; or (2) the plant possesses preformed structural barriers or toxic compounds that confine successful infections to specialized pathogen species; or (3) upon recognition of the attacking pathogen, defense mechanisms are elaborated and the invasion remains localized. All three types of interaction are said to be incompatible, but only the latter resistance mechanism depends on induced responses. Successful pathogen invasion and disease (compatibility) ensue if the preformed plant defenses are inappropriate, the plant does not detect the pathogen, or the activated defense responses are ineffective. In this review, we examine the essential prerequisites for pathogen recognition and the induction of localized defense responses. Preformed defenses are considered elsewhere in this issue. Race-specific pathogen recognition is hypothesized to result from the direct or indirect interaction of the product of a dominant or serodominant plant resistance (R) gene with a product derived from the corresponding dominant pathogen avirulence (Avr) gene. Subsequent signal transduction events are assumed to coordinate the activation of an array of defense responses. This \"simple\" model appears to explain much but begs many questions. For example, R gene products are likely to provide key components for recognition, but how do the distinct classes of R proteins characterized to date activate the defense response? Do different R gene classes activate distinct responses? The regulation of some components of defense mechanisms has been studied in plant cell cultures in response to non-race-specific elicitors, but to what extent do such studies provide a model for R gene function? Plant resistance is often correlated with the activation of specific defense responses, but which (if any) are required to abolish or retard pathogen growth, and how? Which are primary responses and which are secondary? Does the first response involve transcriptional regulation, the activation of preformed enzymes, and/or the opening of ion channels, or are these possibilities nonexclusive? Is the response fine-tuned to the specific pathogen that elicits it? Do the defense responses differ between plant organs, or do they vary according to the attack strategy of the pathogen? To address these questions, we first review the responses that have been correlated with the activation of defense mechanisms in R-Avr gene-dependent resistance and in plant species in which the pathogen never causes disease, that is, nonhost resistance. We then assess the significance of these mechanisms in a few selected examples involving R genes. After considering possible signaling mechanisms and the mechanisms that could initially amplify and subsequently attenuate the response, we discuss the difficulties involved in assessing the functional significance of responses that are correlated with resistance. Some interesting related topics, such as the relationship between R gene structure and function, the significance of disease lesion mimics, and the phenomenon of systemic acquired resistance (SAR), receive limited attention here and are covered elsewhere in this issue. In Figure 1, various induced defense responses encountered by invading microbes are depicted.

The tomato Cf-9 gene confers resistance to infection by races of the fungus Cladosporium fulvum that carry the avirulence gene Avr9. The Cf-9 gene was isolated by transposon tagging with the maize transposable element Dissociation. The DNA sequence of Cf-9 encodes a putative membrane-anchored extracytoplasmic glycoprotein. The predicted protein shows homology to the receptor domain of several receptor-like protein kinases in Arabidopsis, to antifungal polygalacturonase-inhibiting proteins in plants, and to other members of the leucine-rich repeat family of proteins. This structure is consistent with that of a receptor that could bind Avr9 peptide and activate plant defense

Fusarium head blight (FHB) is one of the most destructive diseases of wheat and other cereals worldwide. During infection, the Fusarium fungi produce mycotoxins that represent a high risk to human and animal health. Developing small-molecule inhibitors to specifically reduce mycotoxin levels would be highly beneficial since current treatments unspecifically target the Fusarium pathogen. Culmorin possesses a well-known important synergistically virulence role among mycotoxins, and longiborneol synthase appears to be a key enzyme for its synthesis, thus making longiborneol synthase a particularly interesting target. This study aims to discover potent and less toxic agrochemicals against FHB. These compounds would hamper culmorin synthesis by inhibiting longiborneol synthase. In order to select starting molecules for further investigation, we have conducted a structure-based virtual screening investigation. A longiborneol synthase structural model is first built using homology modeling, followed by molecular dynamics simulations that provided the required input for a protein–ligand ensemble docking procedure. From this strategy, the three most interesting compounds (hits) were selected among the 25 top-ranked docked compounds from a library of 15,000 drug-like compounds. These putative inhibitors of longiborneol synthase provide a sound starting point for further studies involving molecular modeling coupled to biochemical experiments. This process could eventually lead to the development of novel approaches to reduce mycotoxin contamination in harvested grain.

The chronological order of responses to Cladosporium fulvum (Cooke) (Cf) race-specific elicitors was assessed in cotyledons of three near-isogenic tomato (Lycopersicon esculentum Mill.) lines carrying either Cf-9 or Cf-2 or no Cf gene. The responses observed were dependent on the presence of a Cf gene, Avr-gene product dose injected, and the relative humidity (RH) of the growth chamber. At ambient RH, superoxide formation and lipid peroxidation occurred after 2 h (Cf9) and 4 h (Cf2). At elevated RH (98%) and at lower avirulence elicitor dose, Cf-Avr-dependent lipid peroxidation was considerably attenuated. Significant electrolyte leakage occurred by 18 h but only at the lower RH. Total glutathione levels began to increase 2 to 4 h and 4 to 8 h after challenge of Cf9 and Cf2 cells, respectively, and by 48 h reached 665 and 570% of initial levels. A large proportion of this accumulation (87%) was as oxidized glutathione. When the RH was increased to 98%, increases in glutathione levels were strongly attenuated. Increased lipoxygenase enzyme activity was detected 8 h postchallenge in either incompatible interaction. These results indicate that the activation of the Cf-Avr-mediated defense response results in severe oxidative stress.

A mosaic disease caused by Soil-borne cereal mosaic virus (SBCMV) is becoming increasingly important, particularly in winter wheat in Europe. As there are currently no effective cultural practices or practical environmentally friendly chemicals for disease control, host plant resistance is an important objective in breeding programs. However, development of resistant cultivars is slow owing to difficulties in germplasm screening for resistance. Therefore, there is a need to identify molecular markers linked to SBCMV-resistance gene(s), so that quick and accurate laboratory-based marker-assisted selection rather than prolonged field-based screens for resistance can be used in developing resistant cultivars. We previously demonstrated that resistance to SBCMV in Triticum aestivum 'Cadenza' is controlled by a single locus. In this work, we used AFLP and microsatellite technology to map this resistance locus, with the proposed name Sbm1, to the distal end of chromosome 5DL. Interestingly, several expressed disease-resistance gene analogues also map to this gene-rich region on 5DL. Closely linked (~17 cM interval) markers, BARC110 and WMC765, RRES01 and BARC144, that flank Sbm1 will be very useful in breeding for selection of germplasm carrying Sbm1.

The tomato Cf-9 gene confers resistance to races of the fungal pathogen Cladosporium fulvum expressing the Avr9 gene. cDNA amplified fragment length polymorphism analysis was used to display transcripts whose expression is rapidly altered during the Avr9- and Cf-9-mediated defense response in tobacco cell cultures. Diphenyleneiodonium was used to abolish the production of active oxygen species during gene induction. Of 30,000 fragments inspected, 290 showed altered abundance, of which 263 were induced independently of active oxygen species. cDNA clones were obtained for 13 ACRE (for Avr9/Cf-9 rapidly elicited) genes. ACRE gene induction occurred in the presence of cycloheximide. Avr9 induced ACRE gene expression in leaves. Surprisingly, ACRE genes were also rapidly but transiently induced in leaves in response to other stresses. The amino acid sequences of some ACRE proteins are homologous to sequences of known proteins such as ethylene response element binding protein transcription factors, the N resistance protein, a calcium binding protein, 13-lipoxygenase, and a RING-H2 zinc finger protein. Rapid induction of ACRE genes suggests that they play a pivotal role during plant defense responses.

Cf-9 confers resistance to tomato seedlings and mature plants against Cladosporium fulvum races expressing the Avr9 elicitor. It is the central member of a cluster of five paralogous genes in an introgressed segment of chromosome 1 derived from Lycopersicon pimpinellifolium. The other four genes have been named Hcr9-9A, Hcr9-9B, Hcr9-9D, and Hcr9-9E. Hcr9-9B, here designated Cf-9B, encodes weaker resistance than Cf-9, recognizes a different elicitor, and protects only mature plants from infection. The onset of Cf-9B-mediated resistance and the molecular basis for its developmental control were investigated in this study. Fungal inoculation of tomato plants containing reciprocal Cf-9/Cf-9B promoter-coding region swaps, analysis of tomato plants containing promoter-gusA fusions, and a reverse transcriptase-polymerase chain reaction study of Cf-9 and Cf-9B transcripts in tomato plants suggested that transcriptional control of Cf-9B did not account for the late onset of Cf-9B-mediated resistance. Alternative explanations for the onset of Cf-9B-mediated resistance in mature plants are discussed.

Gamma-ray bursts (GRBs) are brief flashes of γ-rays and are considered to be the most energetic explosive phenomena in the Universe1. The emission from GRBs comprises a short (typically tens of seconds) and bright prompt emission, followed by a much longer afterglow phase. During the afterglow phase, the shocked outflow—produced by the interaction between the ejected matter and the circumburst medium—slows down, and a gradual decrease in brightness is observed2. GRBs typically emit most of their energy via γ-rays with energies in the kiloelectronvolt-to-megaelectronvolt range, but a few photons with energies of tens of gigaelectronvolts have been detected by space-based instruments3. However, the origins of such high-energy (above one gigaelectronvolt) photons and the presence of very-high-energy (more than 100 gigaelectronvolts) emission have remained elusive4. Here we report observations of very-high-energy emission in the bright GRB 180720B deep in the GRB afterglow—ten hours after the end of the prompt emission phase, when the X-ray flux had already decayed by four orders of magnitude. Two possible explanations exist for the observed radiation: inverse Compton emission and synchrotron emission of ultrarelativistic electrons. Our observations show that the energy fluxes in the X-ray and γ-ray range and their photon indices remain comparable to each other throughout the afterglow. This discovery places distinct constraints on the GRB environment for both emission mechanisms, with the inverse Compton explanation alleviating the particle energy requirements for the emission observed at late times. The late timing of this detection has consequences for the future observations of GRBs at the highest energies

Defense responses mediated by the genetically unlinked Cf-9 and Cf-2 genes were compared with those involving no Cf gene (Cf0). Compatible tomato (Lycopersicon esculentum)-Cladosporium fulvum intercellular washing fluids were injected into tomato cotyledons, and the kinetics of responses was monitored under conditions of 70 and 98% relative humidity. The latter conditions suppressed the normal macroscopic responses. For the Cf-9-Avr9 interaction, stomatal opening was induced within 3 to 4 h and after 9 h mesophyll cell death commenced. A burst of ethylene production occurred between 9 and 12.5 h and remained elevated. Free salicylic acid levels increased after 12 h, peaked at 24 h, and thereafter declined. For the Cf-2-Avr2 interaction, stomata became plugged after 8 h, and salicylic acid and ethylene levels increased by 12 and 18 h, respectively, and thereafter declined. Host cell death commenced around vascular tissue by 24 h. Cell death in both incompatible interactions was frequently preceded by cell enlargement. For Cf0-injected plants, no significant responses were detected. High humidity delayed and reduced the Cf-Avr-gene-dependent cell death and ethylene synthesis, whereas induced salicylic acid levels were unaffected for Cf-2-Avr2 and reduced in magnitude only for Cf-9-Avr9.