Effects of an entomopathogenic fungus on the reproductive potential of Drosophila males.

While mortality is often the primary focus of pathogen virulence, non-lethal consequences, particularly for male reproductive fitness, are less understood; however, they are essential for understanding how sexual selection contributes to promoting resistance. We investigated how the fungal pathogen Metarhizium brunneum affects mating ability, fertility, and seminal fluid protein (SFP) expression of male Drosophila melanogaster paired with highly receptive virgin females in non-competitive settings. Depending on sex and dose, there was a 3-6-day incubation period after infection, followed by an abrupt onset of mortality. Meanwhile, the immune response was strongly induced already 38 h after infection and continued to increase as infection progressed. Latency to mate somewhat increased during the incubation period compared to sham-treated males, but even on Day 5 post infection >90% of infected males mated within 2 h. During the incubation period, M. brunneum infection reduced male reproductive potential (the number of offspring sired without mate limitation) by 11%, with no clear increase over time. Approaching the end of the incubation period, infected males had lower ability to convert number of mating opportunities into number of offspring. After repeated mating, infected males had lower SFP expression than sham controls, more so in males that mated with few mates 24 h earlier. Overall, despite strong activation of the immune response, males' mating ability and fertility remained surprisingly little affected by the fungal infection, even shortly before the onset of mortality. This suggests that the selection for resistance acts mainly through mortality, and the scope for fertility selection to enhance resistance in non-competing settings is rather limited.

How plants manage pathogen infection.

To combat microbial pathogens, plants have evolved specific immune responses that can be divided into three essential steps: microbial recognition by immune receptors, signal transduction within plant cells, and immune execution directly suppressing pathogens. During the past three decades, many plant immune receptors and signaling components and their mode of action have been revealed, markedly advancing our understanding of the first two steps. Activation of immune signaling results in physical and chemical actions that actually stop pathogen infection. Nevertheless, this third step of plant immunity is under explored. In addition to immune execution by plants, recent evidence suggests that the plant microbiota, which is considered an additional layer of the plant immune system, also plays a critical role in direct pathogen suppression. In this review, we summarize the current understanding of how plant immunity as well as microbiota control pathogen growth and behavior and highlight outstanding questions that need to be answered.

Small holes, big impact: Stomata in plant-pathogen-climate epic trifecta.

The regulation of stomatal aperture opening and closure represents an evolutionary battle between plants and pathogens, characterized by adaptive strategies that influence both plant resistance and pathogen virulence. The ongoing climate change introduces further complexity, affecting pathogen invasion and host immunity. This review delves into recent advances on our understanding of the mechanisms governing immunity-related stomatal movement and patterning with an emphasis on the regulation of stomatal opening and closure dynamics by pathogen patterns and host phytocytokines. In addition, the review explores how climate changes impact plant-pathogen interactions by modulating stomatal behavior. In light of the pressing challenges associated with food security and the unpredictable nature of climate changes, future research in this field, which includes the investigation of spatiotemporal regulation and engineering of stomatal immunity, emerges as a promising avenue for enhancing crop resilience and contributing to climate control strategies.

Virulence decomposition for bifurcating infections.

A fundamental goal in infection biology is to understand the emergence of variation in pathogen virulence-here defined as the decrease in host fitness caused by a pathogen. To uncover the sources of such variation, virulence can be decomposed into both host- and pathogen-associated components. However, decomposing virulence can be challenging owing to complex within-host pathogen dynamics such as bifurcating infections, which recently received increased empirical and theoretical attention. Bifurcating infections are characterized by the emergence of two distinct infection types: (i) terminal infections with high pathogen loads resulting in rapid host death, and (ii) persistent infections with lower loads and delayed host death. Here, we propose to use discrete mixture models to perform separate virulence decompositions for each infection type. Using this approach, we reanalysed a recently published experimental dataset on bacterial load and survival in Drosophila melanogaster. This analysis revealed several advantages of the new approach, most importantly the generation of a more comprehensive picture of the varying sources of virulence in different bacterial species. Beyond this application, our approach could provide valuable information for ground-truthing and improving theoretical models of within-host infection dynamics, which are developed to predict variation in infection outcome and pathogen virulence.

The function of plant PR1 and other members of the CAP protein superfamily in plant-pathogen interactions.

The pathogenesis-related (PR) proteins of plants have originally been identified as proteins that are strongly induced upon biotic and abiotic stress. These proteins fall into 17 distinct classes (PR1-PR17). The mode of action of most of these PR proteins has been well characterized, except for PR1, which belongs to a widespread superfamily of proteins that share a common CAP domain. Proteins of this family are not only expressed in plants but also in humans and in many different pathogens, including phytopathogenic nematodes and fungi. These proteins are associated with a diverse range of physiological functions. However, their precise mode of action has remained elusive. The importance of these proteins in immune defence is illustrated by the fact that PR1 overexpression in plants results in increased resistance against pathogens. However, PR1-like CAP proteins are also produced by pathogens and deletion of these genes results in reduced virulence, suggesting that CAP proteins can exert both defensive and offensive functions. Recent progress has revealed that plant PR1 is proteolytically cleaved to release a C-terminal CAPE1 peptide, which is sufficient to activate an immune response. The release of this signalling peptide is blocked by pathogenic effectors to evade immune defence. Moreover, plant PR1 forms complexes with other PR family members, including PR5, also known as thaumatin, and PR14, a lipid transfer protein, to enhance the host's immune response. Here, we discuss possible functions of PR1 proteins and their interactors, particularly in light of the fact that these proteins can bind lipids, which have important immune signalling functions.

Campylobacter fetus releases S-layered and immunoreactive outer membrane vesicles

Abstract The study of outer membrane vesicles (OMVs) became relevant because of theirprobable important role in the transfer of virulence factors to host cells. Campylobacter fetusis mainly a mammal pathogen whose virulence characterization is still limited. The aim of thisstudy was to evaluate and to characterize the secretion of OMVs in this bacterium. By trans-mission electron microscopy, we confirmed the production of OMVs in all the strains assayed.Purified OMVs showed a spherical shape and variable size, although comparable to those ofother gram-negative bacteria. We also confirmed the presence of the S-layer on the surface ofthe OMVs of all the strains assayed with the exception of those derived from the NTCC referencestrain. In addition, we demonstrated their immunoreactivity by the dot-blot assay. Hence, C.fetus OMVs could contribute to the modulation of the host response and constitute a candidateto be evaluated as an adjuvant of current vaccines used in the veterinary field. This work rep-resents a platform to drive future studies towards the role of these subcellular structures in C.fetus-host interaction.

Resumen El estudio de las vesículas de membrana externa (VME) tomó un rol protagónico, yaque se las ha relacionado con la transferencia de factores de virulencia a la célula hospedadora.Campylobacter fetus es, principalmente, un patógeno de mamíferos cuya virulencia solo hasido caracterizada de forma limitada. El objetivo de este trabajo fue evaluar y caracterizar la secreción de VME en esta bacteria. Mediante microscopía electrónica de transmisión confir-mamos la producción espontánea de VME en todas las cepas estudiadas. Las VME purificadasmostraron una morfología esférica y un tama˜no variable, pero compatible con el reporte deotras bacterias gram negativas. Asimismo, hemos demostrado que estas vesículas conservanla capa S en todas las cepas, menos en la cepa de referencia NCTC y hemos confirmado suinmunorreactividad por dot-blot inmunoblot. Estas VME de C. fetus podrían contribuir a la mod-ulación de la respuesta del hospedador y constituir un buen candidato como adyuvante de lasactuales vacunas empleadas en el campo veterinario. Este trabajo representa una plataformapara impulsar estudios futuros en torno al rol de estas estructuras subcelulares en la interfaseC. fetus-hospedador.

Novel chytrid pathogen variants and the global amphibian pet trade.

Global wildlife trade spreads emerging infectious diseases that threaten biodiversity. The amphibian chytrid pathogen Batrachochytrium dendrobatidis (Bd) has caused population declines and species extinctions worldwide except in Asia. Fire-bellied toads (Bombina orientalis), exported in large numbers from Asia, are tolerant of Bd and carry hypervirulent ancestral chytrid BdAsia-1 variants. We assayed the virulence of a new isolate of BdAsia-1 on the model Australasian frog host Litoria caerulea. Infected individuals (n = 15) all showed rapid disease progression culminating in death, whereas sham-inoculated individuals (n = 10) presented no clinical signs of disease and all survived (log rank test, χ2 = 15.6, df = 1, p < 0.0001). The virulence of the new isolate of BdAsia-1 is comparable to the one we assayed previously (χ2 = 0.0, df = 1, p = 0.91). Internationally traded wildlife, even when they appear healthy, can carry hypervirulent variants of pathogens. Once new pathogen variants escape into the environment, native species that have had no opportunity to evolve resistance to them may perish. Our study suggests that hypervirulent pathogens are being spread by the international pet trade. Notifiable wildlife diseases attributable to locally endemic pathogens often fail to generate conservation concern so are rarely subject to border surveillance or import controls. Because of the danger novel variants pose, national border control agencies need to implement disease screening and quarantine protocols to ensure the safety of their endemic fauna.

Variantes Patógenas Nuevas de Quitridios y el Mercado Mundial de Anfibios Mascota Resumen El mercado mundial de fauna dispersa enfermedades infecciosas emergentes que amenazan a la biodiversidad. El quitridio patógeno de anfibios Batrachochytrium dendrobatidis (Bd) ha causado declinaciones poblacionales y la extinción de especies en todo el mundo excepto Asia. El sapo Bombina orientalis, exportado en grandes cantidades desde Asia, es tolerante al Bd y carga genéticamente las variantes ancestrales hipervirulentas de quitridio BdAsia-1. Analizamos la virulencia de una nueva cepa de BdAsia-1 con el modelo de la rana australo-asiática hospedera Litoria caerulea. Todos los individuos infectados (n = 15) mostraron una progresión acelerada de la enfermedad que culminaba con la muerte, mientras que los individuos con inoculación simulada (n = 10) no presentaron señales clínicas de la enfermedad y todos sobrevivieron (prueba log de rango, χ2 = 15.6, df = 1, p < 0.0001). La virulencia de la nueva cepa de BdAsia-1 es comparable a la que analizamos previamente (χ2 = 0.0, df = 1, p = 0.91). La fauna comercializada internacionalmente, incluso cuando parece estar saludable, puede portar variantes hipervirulentas de los patógenos. Una vez que un patógeno nuevo se introduce al ambiente, pueden perecer las especies nativas que no han tenido la oportunidad de evolucionar la resistencia a estos patógenos. Nuestro estudio sugiere que los patógenos hipervirulentos se están dispersando mediante el mercado internacional de mascotas. Con frecuencia las enfermedades silvestres notificables que pueden atribuirse a los patógenos endémicos no generan interés para la conservación, así que rara vez están sujetas a la vigilancia fronteriza o el control de importación. Debido al riesgo que representan las variantes nuevas, las agencias nacionales de control fronterizo necesitan implementar evaluaciones patológicas y protocolos de cuarentena para asegurar la seguridad de su fauna endémica.

Pathogen Moonlighting Proteins: From Ancestral Key Metabolic Enzymes to Virulence Factors.

Moonlighting and multitasking proteins refer to proteins with two or more functions performed by a single polypeptide chain. An amazing example of the Gain of Function (GoF) phenomenon of these proteins is that 25% of the moonlighting functions of our Multitasking Proteins Database (MultitaskProtDB-II) are related to pathogen virulence activity. Moreover, they usually have a canonical function belonging to highly conserved ancestral key functions, and their moonlighting functions are often involved in inducing extracellular matrix (ECM) protein remodeling. There are three main questions in the context of moonlighting proteins in pathogen virulence: (A) Why are a high percentage of pathogen moonlighting proteins involved in virulence? (B) Why do most of the canonical functions of these moonlighting proteins belong to primary metabolism? Moreover, why are they common in many pathogen species? (C) How are these different protein sequences and structures able to bind the same set of host ECM protein targets, mainly plasminogen (PLG), and colonize host tissues? By means of an extensive bioinformatics analysis, we suggest answers and approaches to these questions. There are three main ideas derived from the work: first, moonlighting proteins are not good candidates for vaccines. Second, several motifs that might be important in the adhesion to the ECM were identified. Third, an overrepresentation of GO codes related with virulence in moonlighting proteins were seen.

Pangenomic Analysis of Dickeya dianthicola Strains Related to the Outbreak of Blackleg and Soft Rot of Potato in the United States.

Dickeya dianthicola has caused an outbreak of blackleg and soft rot of potato in the eastern half of the United States since 2015. To investigate genetic diversity of the pathogen, a comparative analysis was conducted on genomes of D. dianthicola strains. Whole genomes of 16 strains from the United States outbreak were assembled and compared with 16 previously sequenced genomes of D. dianthicola isolated from potato or carnation. Among the 32 strains, eight distinct clades were distinguished based on phylogenomic analysis. The outbreak strains were grouped into three clades, with the majority of the strains in clade I. Clade I strains were unique and homogeneous, suggesting a recent incursion of this strain into potato production from alternative hosts or environmental sources. The pangenome of the 32 strains contained 6,693 genes, 3,377 of which were core genes. By screening primary protein subunits associated with virulence from all U.S. strains, we found that many virulence-related gene clusters, such as plant cell wall degrading enzyme genes, flagellar and chemotaxis related genes, two-component regulatory genes, and type I/II/III secretion system genes, were highly conserved but that type IV and type VI secretion system genes varied. The clade I strains encoded two clusters of type IV secretion systems, whereas the clade II and III strains encoded only one cluster. Clade I and II strains encoded one more VgrG/PAAR spike protein than did clade III. Thus, we predicted that the presence of additional virulence-related genes may have enabled the unique clade I strain to become predominant in the U.S. outbreak.

Current status and future prospects of grapevine anthracnose caused by Elsinoe ampelina: An important disease in humid grape-growing regions.

Anthracnose, caused by Elsinoe ampelina, is one of the most destructive diseases of grapevines worldwide, especially in humid areas. E. ampelina mainly infects young tissues starting from shoots to berries and affects vine vigour and berry yield. The occurrence and the role of the sexual stage in the disease cycle and the grapevine-E. ampelina interaction remain poorly understood. However, the recent genome sequence data of E. ampelina provides the basis for further studies to understand its evolution, pathogenicity mechanisms, and effector repertoire. New studies on E. ampelina have been conducted in recent years. In this pathogen profile, we present a comprehensive literature review of E. ampelina to summarize the findings on its aetiology, infection mechanisms, genome, pathogenicity, and host resistance. TAXONOMY: Elsinoe ampelina Shear; Kingdom Fungi; Phylum Ascomycota; Subphylum Pezizomycotina; Class Dothideomycetes; Subclass Dothideomycetidae; Order Myriangiales Starbäck; Family Elsinoaceae Höhnel; Genus Elsinoe Racib. HOST RANGE: E. ampelina only infects Vitis species and hybrids. DISTRIBUTION: The grapevine anthracnose is distributed worldwide but is most prevalent in Argentina, Australia, Brazil, Canada, China, India, Japan, Korea, New Zealand, South Africa, Thailand, USA, and Uruguay. DISEASE SYMPTOMS: E. ampelina causes slightly abundant depressed spots on young leaves, petioles, stems, tendrils, rachises, and berries. Under severe infection conditions, early defoliation, berry dropping, and delayed berry development and ripening may occur. GENOME: The genomes of two E. ampelina isolates, YL-1 and CECT 20119, are publicly released with 8,057 and 10,207 predicted genes, respectively.

The Microbiota and Gut-Related Disorders: Insights from Animal Models.

Over the past decade, the scientific committee has called for broadening our horizons in understanding host-microbe interactions and infectious disease progression. Owing to the fact that the human gut harbors trillions of microbes that exhibit various roles including the production of vitamins, absorption of nutrients, pathogen displacement, and development of the host immune system, particular attention has been given to the use of germ-free (GF) animal models in unraveling the effect of the gut microbiota on the physiology and pathophysiology of the host. In this review, we discuss common methods used to generate GF fruit fly, zebrafish, and mice model systems and highlight the use of these GF model organisms in addressing the role of gut-microbiota in gut-related disorders (metabolic diseases, inflammatory bowel disease, and cancer), and in activating host defense mechanisms and amending pathogenic virulence.

Drosophila as a Model Organism in Host-Pathogen Interaction Studies.

Owing to the genetic similarities and conserved pathways between a fruit fly and mammals, the use of the Drosophila model as a platform to unveil novel mechanisms of infection and disease progression has been justified and widely instigated. Gaining proper insight into host-pathogen interactions and identifying chief factors involved in host defense and pathogen virulence in Drosophila serves as a foundation to establish novel strategies for infectious disease prevention and control in higher organisms, including humans.

Differential house finch leukocyte profiles during experimental infection with Mycoplasma gallisepticum isolates of varying virulence.

Leukocyte differentials are a useful tool for assessing systemic immunological changes during pathogen infections, particularly for non-model species. To date, no study has explored how experimental infection with a common bacterial pathogen, Mycoplasma gallisepticum (MG), influences the course and strength of haematological changes in the natural songbird host, house finches. Here we experimentally inoculated house finches with MG isolates known to vary in virulence, and quantified the proportions of circulating leukocytes over the entirety of infection. First, we found significant temporal effects of MG infection on the proportions of most cell types, with strong increases in heterophil and monocyte proportions during infection. Marked decreases in lymphocyte proportions also occurred during infection, though these proportional changes may simply be driven by correlated increases in other leukocytes. Second, we found significant effects of isolate virulence, with the strongest changes in cell proportions occurring in birds inoculated with the higher virulence isolates, and almost no detectable changes relative to sham treatment groups in birds inoculated with the lowest virulence isolate. Finally, we found that variation in infection severity positively predicted the proportion of circulating heterophils and lymphocytes, but the strength of these correlations was dependent on isolate. Taken together, these results indicate strong haematological changes in house finches during MG infection, with markedly different responses to MG isolates of varying virulence. These results are consistent with the possibility that evolved virulence in house finch MG results in higher degrees of immune stimulation and associated immunopathology, with potential direct benefits for MG transmission. RESEARCH HIGHLIGHTS House finches show a marked pro-inflammatory response to M. gallisepticum infection. Virulent pathogen isolates produce stronger finch white blood cell responses. Among birds, stronger white blood cell responses are associated with higher infection severity.

The translucens group of Xanthomonas translucens: Complicated and important pathogens causing bacterial leaf streak on cereals.

Xanthomonas translucens is a group of gram-negative bacteria that can cause important diseases in cereal crops and forage grasses. Different pathovars have been defined according to their host ranges, and molecular and biochemical characteristics. Pathovars have been placed into two major groups: translucens and graminis. The translucens group contains the pathovars causing bacterial leaf streak (BLS) on cereal crops such as wheat, barley, triticale, rye, and oat. In recent years, BLS has re-emerged as a major problem for many wheat- and barley-producing areas worldwide. The biology of the pathogens and the host-pathogen interactions in cereal BLS diseases were poorly understood. However, recent genome sequence data have provided an insight into the bacterial phylogeny and identification and pathogenicity/virulence. Furthermore, identification of sources of resistance to BLS and mapping of the resistance genes have been initiated. TAXONOMY: Kingdom Bacteria; Phylum Proteobacteria; Class Gammaproteobacteria; Order Xanthomonadales; Family Xanthomonadaceae; Genus Xanthomonas; Species X. translucens; translucens group pathovars: undulosa, translucens, cerealis, hordei, and secalis; graminis group pathovars: arrhenatheri, graminis, poae, phlei; newly established pathovar: pistaciae. HOST RANGE: X. translucens mainly infects plant species in the Poaceae with the translucens group on cereal crop species and the graminis group on forage grass species. However, some strains have been isolated from, and are able to infect, ornamental asparagus and pistachio trees. Most pathovars have a narrow host range, while a few can infect a broad range of hosts. GENOME: The complete genome sequence is available for two X. translucens pv. undulosa strains and one pv. translucens strain. A draft genome sequence is also available for at least one strain from each pathovar. The X. translucens pv. undulosa strain Xt4699 was the first to have its complete genome sequenced, which consists of 4,561,137 bp with total GC content approximately at 68% and 3,528 predicted genes. VIRULENCE MECHANISMS: Like most xanthomonads, X. translucens utilizes a type III secretion system (T3SS) to deliver a suite of T3SS effectors (T3Es) inside plant cells. Transcription activator-like effectors, a special group of T3Es, have been identified in most of the X. translucens genomes, some of which have been implicated in virulence. Genetic factors determining host range virulence have also been identified.

Phagomimetic action of antibiotics: Revisited. How do antibiotics know where to go?

Phagocytic cells know exactly where an infection is by following chemotactic signals. The phagocytosis of bacteria results in a 'respiratory burst' in which superoxide radicals are released. We have previously compared the release of reactive oxygen species (ROS) by antibiotics, during electron transfer reactions, to this event. Antibiotics in their normal bacterial environment, and ROS, are both increasingly implicated in purposeful signalling functions, rather than their more widely known roles in bacterial killing and molecular damage. Here, we extend our comparison between antibiotics and phagocytic cells to propose that antibiotics actively accumulate at a site of pathogen infection or tumour growth. A common link being virulent cellular growth. When this occurs, new proteins are secreted, aberrant iron acquisition takes place, and lipocalins are released. Each provide a mechanism by which antibiotics can bind, and be retained, at an active site of pathogen infection or tumour growth.

Ancestral chytrid pathogen remains hypervirulent following its long coevolution with amphibian hosts.

Many amphibian species around the world, except in Asia, suffer morbidity and mortality when infected by the emerging infectious pathogen Batrachochytrium dendrobatidis (Bd). A lineage of the amphibian chytrid fungus isolated from South Korean amphibians (BdAsia-1) is evolutionarily basal to recombinant global pandemic lineages (BdGPL) associated with worldwide amphibian population declines. In Asia, the Bd pathogen and its amphibian hosts have coevolved over 100 years or more. Thus, resilience of Asian amphibian populations to infection might result from attenuated virulence of endemic Bd lineages, evolved immunity to the pathogen or both. We compared susceptibilities of an Australasian amphibian, Litoria caerulea, known to lack resistance to BdGPL, with those of three Korean species, Bufo gargarizans, Bombina orientalis and Hyla japonica, after inoculation with BdAsia-1, BdGPL or a blank solution. Subjects became infected in all experimental treatments but Korean species rapidly cleared themselves of infection, regardless of Bd lineage. They survived with no apparent secondary effects. By contrast, L. caerulea, after infection by either BdAsia-1 or BdGPL, suffered deteriorating body condition and carried progressively higher Bd loads over time. Subsequently, most subjects died. Comparing their effects on L. caerulea, BdAsia-1 induced more rapid disease progression than BdGPL. The results suggest that genomic recombination with other lineages was not necessary for the ancestral Bd lineage to evolve hypervirulence over its long period of coevolution with amphibian hosts. The pathogen's virulence may have driven strong selection for immune responses in endemic Asian amphibian host species.

Structural and functional insights into the modulation of the activity of a flax cytokinin oxidase by flax rust effector AvrL567-A.

During infection, plant pathogens secrete effector proteins to facilitate colonization. In comparison with our knowledge of bacterial effectors, the current understanding of how fungal effectors function is limited. In this study, we show that the effector AvrL567-A from the flax rust fungus Melampsora lini interacts with a flax cytosolic cytokinin oxidase, LuCKX1.1, using both yeast two-hybrid and in planta bimolecular fluorescence assays. Purified LuCKX1.1 protein shows catalytic activity against both N6-(Δ2-isopentenyl)-adenine (2iP) and trans-zeatin (tZ) substrates. Incubation of LuCKX1.1 with AvrL567-A results in increased catalytic activity against both substrates. The crystal structure of LuCKX1.1 and docking studies with AvrL567-A indicate that the AvrL567 binding site involves a flexible surface-exposed region that surrounds the cytokinin substrate access site, which may explain its effect in modulating LuCKX1.1 activity. Expression of AvrL567-A in transgenic flax plants gave rise to an epinastic leaf phenotype consistent with hormonal effects, although no difference in overall cytokinin levels was observed. We propose that, during infection, plant pathogens may differentially modify the levels of extracellular and intracellular cytokinins.

Pathogen-produced catalase affects immune priming: A potential pathogen strategy.

Immune priming in invertebrates occurs when the first contact with a pathogen/parasite enhances resistance after a second encounter with the same strain or species. Although the mechanisms are not well understood, there is evidence that priming the immune response of some hosts leads to greater pro-oxidant production. Parasites, in turn, might counteract the host attack with antioxidants. Virulent pathogen strains may therefore mask invertebrate immune priming. For example, different parasite species overexpress catalase as a virulence factor to resist host pro-oxidants, possibly impairing the immune priming response. The aim of this study was firstly to evaluate the specificity of immune priming in Tenebrio molitor when facing homologous and heterologous challenges. Secondly, homologous challenges were carried out with two Metarhizium anisopliae strains (Ma10 and CAT). The more virulent strain (CAT) overexpresses catalase, an antioxidant that perhaps impairs a host immune response mediated by reactive oxygen species (ROS). Indeed, T. molitor larvae exhibited better immune priming (survival) in response to the Ma10 than CAT homologous challenge. Moreover, the administration of paraquat, an ROS-promoting agent, favoured survival of the host upon exposure to each fungal strain. We propose that some pathogens likely overcome pro-oxidant-mediated immune priming defences by producing antioxidants such as catalase.

Multifaceted Impacts of Bacteriophages in the Plant Microbiome.

Plant-associated bacteria face multiple selection pressures within their environments and have evolved countless adaptations that both depend on and shape bacterial phenotype and their interaction with plant hosts. Explaining bacterial adaptation and evolution therefore requires considering each of these forces independently as well as their interactions. In this review, we examine how bacteriophage viruses (phages) can alter the ecology and evolution of plant-associated bacterial populations and communities. This includes influencing a bacterial population's response to both abiotic and biotic selection pressures and altering ecological interactions within the microbiome and between the bacteria and host plant. We outline specific ways in which phages can alter bacterial phenotype and discuss when and how this might impact plant-microbe interactions, including for plant pathogens. Finally, we highlight key open questions in phage-bacteria-plant research and offer suggestions for future study.

Polyketide synthases of Diaporthe helianthi and involvement of DhPKS1 in virulence on sunflower.

BACKGROUND: The early phases of Diaporthe helianthi pathogenesis on sunflower are characterized by the production of phytotoxins that may play a role in host colonisation. In previous studies, phytotoxins of a polyketidic nature were isolated and purified from culture filtrates of virulent strains of D. helianthi isolated from sunflower. A highly aggressive isolate (7/96) from France contained a gene fragment of a putative nonaketide synthase (lovB) which was conserved in a virulent D. helianthi population. RESULTS: In order to investigate the role of polyketide synthases in D. helianthi 7/96, a draft genome of this isolate was examined. We were able to find and phylogenetically analyse 40 genes putatively coding for polyketide synthases (PKSs). Analysis of their domains revealed that most PKS genes of D. helianthi are reducing PKSs, whereas only eight lacked reducing domains. Most of the identified PKSs have orthologs shown to be virulence factors or genetic determinants for toxin production in other pathogenic fungi. One of the genes (DhPKS1) corresponded to the previously cloned D. helianthi lovB gene fragment and clustered with a nonribosomal peptide synthetase (NRPS) -PKS hybrid/lovastatin nonaketide like A. nidulans LovB. We used DhPKS1 as a case study and carried out its disruption through Agrobacterium-mediated transformation in the isolate 7/96. D. helianthi DhPKS1 deleted mutants were less virulent to sunflower compared to the wild type, indicating a role for this gene in the pathogenesis of the fungus. CONCLUSION: The PKS sequences analysed and reported here constitute a new genomic resource that will be useful for further research on the biology, ecology and evolution of D. helianthi and generally of fungal plant pathogens.