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This work dissects the tripartite horizontal transfer of ToxA , a gene that has a direct negative impact on global wheat yields. Defining the extent of horizontally transferred DNA is important because it can provide clues to the mechanisms that facilitate HGT. Our analysis of ToxA and its surrounding 14 kb suggests that this gene was horizontally transferred in two independent events, with one event likely facilitated by a type II DNA transposon. These horizontal transfer events are now in various processes of decay in each species due to the repeated insertion of new transposons and subsequent rounds of targeted mutation by a fungal genome defense mechanism known as repeat induced point mutation. This work highlights the role that HGT plays in the evolution of host adaptation in eukaryotic pathogens. It also increases the growing body of evidence indicating that transposons facilitate adaptive HGT events between fungi present in similar environments and hosts. Most known examples of horizontal gene transfer (HGT) between eukaryotes are ancient. These events are identified primarily using phylogenetic methods on coding regions alone. Only rarely are there examples of HGT where noncoding DNA is also reported. The gene encoding the wheat virulence protein ToxA and the surrounding 14 kb is one of these rare examples. ToxA has been horizontally transferred between three fungal wheat pathogens ( Parastagonospora nodorum , Pyrenophora tritici- repentis , and Bipolaris sorokiniana ) as part of a conserved ∼14 kb element which contains coding and noncoding regions. Here we used long-read sequencing to define the extent of HGT between these three fungal species. Construction of near-chromosomal-level assemblies enabled identification of terminal inverted repeats on either end of the 14 kb region, typical of a type II DNA transposon. This is the first description of ToxA with complete transposon features, which we call ToxhAT. In all three species, ToxhAT resides in a large (140-to-250 kb) transposon-rich genomic island which is absent in isolates that do not carry the gene (annotated here as toxa − ). We demonstrate that the horizontal transfer of ToxhAT between P. tritici-repentis and P. nodorum occurred as part of a large (∼80 kb) HGT which is now undergoing extensive decay. In B. sorokiniana , in contrast, ToxhAT and its resident genomic island are mobile within the genome. Together, these data provide insight into the noncoding regions that facilitate HGT between eukaryotes and into the genomic processes which mask the extent of HGT between these species. IMPORTANCE This work dissects the tripartite horizontal transfer of ToxA , a gene that has a direct negative impact on global wheat yields. Defining the extent of horizontally transferred DNA is important because it can provide clues to the mechanisms that facilitate HGT. Our analysis of ToxA and its surrounding 14 kb suggests that this gene was horizontally transferred in two independent events, with one event likely facilitated by a type II DNA transposon. These horizontal transfer events are now in various processes of decay in each species due to the repeated insertion of new transposons and subsequent rounds of targeted mutation by a fungal genome defense mechanism known as repeat induced point mutation. This work highlights the role that HGT plays in the evolution of host adaptation in eukaryotic pathogens. It also increases the growing body of evidence indicating that transposons facilitate adaptive HGT events between fungi present in similar environments and hosts.

The plant epidermis is the first line of plant defense against pathogen invasion, and likely contains important regulatory proteins related to the plant–pathogen interaction. This study aims to identify the candidates of these regulatory proteins expressed in the plant epidermis. We performed comparative proteomic studies to identify rapidly and locally expressed proteins in the leaf epidermis inoculated with fungal phytopathogen. The conidia solutions were dropped onto the Arabidopsis leaf surface, and then, we collected the epidermal tissues from inoculated and mock-treated leaves at 4 and 24 hpi. The label-free quantification methods showed that expressions of Arabidopsis proteins, which are related to defense signals, such as BAK1, MKK5, receptor-like protein kinases, transcription factors, and stomatal functions, were rapidly induced in the epidermal tissues of inoculated leaves. In contrast, most of them were not differentially regulated by fugal inoculation in the whole leaves. These findings clearly indicate that epidermal proteomics can monitor locally expressed proteins in inoculated areas of plant tissues. We also identified the 61 fungal proteins, including effector-like proteins specifically expressed on the Arabidopsis epidermis. Our new findings suggested that epidermal proteomics is useful for understanding the local expressions of plant and fungal proteins related to their interactions.

Tree diseases constitute a significant threat to biodiversity worldwide. Pathogen discovery in natural habitats is of vital importance to understanding current and future threats and prioritising efforts towards developing disease management strategies. Ash dieback is a fungal disease of major conservational concern that is infecting common ash trees, Fraxinus excelsior , in Europe. The disease is caused by a non-native fungal pathogen, Hymenoscyphus fraxineus . Other dieback causing-species have not previously been identified in the genus Hymenoscyphus . Here, we discover the pathogenicity potential of two newly identified related species of Asian origin, H. koreanus and H. occultus , and one Europe-native related species, H. albidus . We sequence the genomes of all three Hymenoscyphus species and compare them to that of H. fraxineus . Phylogenetic analysis of core eukaryotic genes identified H. albidus and H. koreanus as sister species, whilst H. occultus diverged prior to these and H. fraxineus . All four Hymenoscyphus genomes are of comparable size (55–62 Mbp) and GC contents (42–44%) and encode for polymorphic secretomes. Surprisingly, 1133 predicted secreted proteins are shared between the ash dieback pathogen H. fraxineus and the three related Hymenoscyphus endophytes. Amongst shared secreted proteins are cell death-inducing effector candidates, such as necrosis, and ethylene-inducing peptide 1-like proteins, Nep1-like proteins, that are upregulated during in planta growth of all Hymenoscyphus species. Indeed, pathogenicity tests showed that all four related Hymenoscyphus species develop pathogenic growth on European ash stems, with native H. albidus being the least virulent. Our results identify the threat Hymenoscypohus species pose to the survival of European ash trees, and highlight the importance of promoting pathogen surveillance in environmental landscapes. Identifying new pathogens and including them in the screening for durable immunity of common ash trees is key to the long-term survival of ash in Europe.

The first meeting of the CIFAR Fungal Kingdom: Threats & Opportunities research program saw the congregation of experts on fungal biology to address the most pressing threats fungi pose to global health, agriculture, and biodiversity. This report covers the research discussed during the meeting and the advancements made toward mitigating the devastating impact of fungi on plants, animals, and humans.

In an experiment that directly manipulated grassland plant species richness and composition, decreased plant species richness (\"diversity\") increased pathogen load (the percentage of leaf area infected by species-specific foliar pathogens across the plant community) in 1998. Pathogen load was almost three times greater in the average mono-culture than in the average plot planted with 24 grassland plant species, an approximately natural diversity. Eleven individual diseases increased in severity (percentage of leaf area infected by a single disease) at lower plant species richness, and severity of only one disease was positively correlated with diversity. For 10 of the 11 diseases whose severity was negatively related to diversity, disease severity was positively correlated with host abundance, and in six of these cases, species diversity had no effect on disease severity after controlling for the effects of host abundance. These results suggest that increased abundances of individual host species at lower species diversity increased disease transmission and severity. In 1996 and 1997, similar results for a smaller number of diseases sampled were found in this experiment and another similar one. Although the effect of diversity on disease was highly significant, considerable variance in pathogen load remained among plots of a given diversity level. Much of this residual variance was explained by community characteristics that were a function of the species composition of the communities (the identity of species present vs. those lost). Specifically, communities that lost less disease-prone species had higher pathogen loads; this effect explained more variance in pathogen load than did diversity. Also, communities that lost the species dominant at high diversity had higher pathogen loads, presumably because relaxed competition allowed greater increases in host abundances, but this effect was weak. Among plant species, disease proneness appeared to be determined more by regional than local processes, because it was better correlated with frequency of the plant species' populations across the region than with local abundance or frequency across the state. In total, our results support the hypothesis that decreased species diversity will increase foliar pathogen load if this increases host abundance and, therefore, disease transmission. Additionally, changes in community characteristics determined by species composition will strongly influence pathogen load.

The fungal kingdom includes at least 6 million eukaryotic species and is remarkable with respect to its profound impact on global health, biodiversity, ecology, agriculture, manufacturing, and biomedical research. Approximately 625 fungal species have been reported to infect vertebrates, 200 of which can be human associated, either as commensals and members of our microbiome or as pathogens that cause infectious diseases. These organisms pose a growing threat to human health with the global increase in the incidence of invasive fungal infections, prevalence of fungal allergy, and the evolution of fungal pathogens resistant to some or all current classes of antifungals. The fungal kingdom includes at least 6 million eukaryotic species and is remarkable with respect to its profound impact on global health, biodiversity, ecology, agriculture, manufacturing, and biomedical research. Approximately 625 fungal species have been reported to infect vertebrates, 200 of which can be human associated, either as commensals and members of our microbiome or as pathogens that cause infectious diseases. These organisms pose a growing threat to human health with the global increase in the incidence of invasive fungal infections, prevalence of fungal allergy, and the evolution of fungal pathogens resistant to some or all current classes of antifungals. More broadly, there has been an unprecedented and worldwide emergence of fungal pathogens affecting animal and plant biodiversity. Approximately 8,000 species of fungi and Oomycetes are associated with plant disease. Indeed, across agriculture, such fungal diseases of plants include new devastating epidemics of trees and jeopardize food security worldwide by causing epidemics in staple and commodity crops that feed billions. Further, ingestion of mycotoxins contributes to ill health and causes cancer. Coordinated international research efforts, enhanced technology translation, and greater policy outreach by scientists are needed to more fully understand the biology and drivers that underlie the emergence of fungal diseases and to mitigate against their impacts. Here, we focus on poignant examples of emerging fungal threats in each of three areas: human health, wildlife biodiversity, and food security.

Eukaryotic filamentous plant pathogens secrete effector proteins that modulate the host cell to facilitate infection. Computational effector candidate identification and subsequent functional characterization delivers valuable insights into plant–pathogen interactions. However, effector prediction in fungi has been challenging due to a lack of unifying sequence features such as conserved N‐terminal sequence motifs. Fungal effectors are commonly predicted from secretomes based on criteria such as small size and cysteine‐rich, which suffers from poor accuracy. We present EffectorP which pioneers the application of machine learning to fungal effector prediction. EffectorP improves fungal effector prediction from secretomes based on a robust signal of sequence‐derived properties, achieving sensitivity and specificity of over 80%. Features that discriminate fungal effectors from secreted noneffectors are predominantly sequence length, molecular weight and protein net charge, as well as cysteine, serine and tryptophan content. We demonstrate that EffectorP is powerful when combined with in planta expression data for predicting high‐priority effector candidates. EffectorP is the first prediction program for fungal effectors based on machine learning. Our findings will facilitate functional fungal effector studies and improve our understanding of effectors in plant–pathogen interactions. EffectorP is available at http://effectorp.csiro.au.

Invasive species present significant threats to global agriculture, although how the magnitude and distribution of the threats vary between countries and regions remains unclear. Here, we present an analysis of almost 1,300 known invasive insect pests and pathogens, calculating the total potential cost of these species invading each of 124 countries of the world, as well as determining which countries present the greatest threat to the rest of the world given their trading partners and incumbent pool of invasive species. We find that countries vary in terms of potential threat from invasive species and also their role as potential sources, with apparently similar countries sometimes varying markedly depending on specifics of agricultural commodities and trade patterns. Overall, the biggest agricultural producers (China and the United States) could experience the greatest absolute cost from further species invasions. However, developing countries, in particular, Sub-Saharan African countries, appear most vulnerable in relative terms. Furthermore, China and the United States represent the greatest potential sources of invasive species for the rest of the world. The analysis reveals considerable scope for ongoing redistribution of known invasive pests and highlights the need for international cooperation to slow their spread.

Fungal response to any stress is intricate, specific, and multilayered, though it employs only a few evolutionarily conserved regulators. This comes with the assumption that one regulator operates more than one stress-specific response. Although the assumption holds true, the current understanding of molecular mechanisms that drive response specificity and adequacy remains rudimentary. Deciphering the response of fungi to oxidative stress may help fill those knowledge gaps since it is one of the most encountered stress types in any kind of fungal niche. Data have been accumulating on the roles of the HOG pathway and Yap1- and Skn7-related pathways in mounting distinct and robust responses in fungi upon exposure to oxidative stress. Herein, we review recent and most relevant studies reporting the contribution of each of these pathways in response to oxidative stress in pathogenic and opportunistic fungi after giving a paralleled overview in two divergent models, the budding and fission yeasts. With the concept of stress-specific response and the importance of reactive oxygen species in fungal development, we first present a preface on the expanding domain of redox biology and oxidative stress.

Agricultural ecosystems are composed of genetically depauperate populations of crop plants grown at a high density and over large spatial scales, with the regional composition of crop species changing little from year to year. These environments are highly conducive for the emergence and dissemination of pathogens. The uniform host populations facilitate the specialization of pathogens to particular crop cultivars and allow the build-up of large population sizes. Population genetic and genomic studies have shed light on the evolutionary mechanisms underlying speciation processes, adaptive evolution and long-distance dispersal of highly damaging pathogens in agro-ecosystems. These studies document the speed with which pathogens evolve to overcome crop resistance genes and pesticides. They also show that crop pathogens can be disseminated very quickly across and among continents through human activities. In this review, we discuss how the peculiar architecture of agro-ecosystems facilitates pathogen emergence, evolution and dispersal. We present four example pathosystems that illustrate both pathogen specialization and pathogen speciation, including different time frames for emergence and different mechanisms underlying the emergence process. Lastly, we argue for a re-design of agro-ecosystems that embraces the concept of dynamic diversity to improve their resilience to pathogens. This article is part of the themed issue ‘Tackling emerging fungal threats to animal health, food security and ecosystem resilience’.