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Summary 513 I. Introduction 513 II. Continua in plant host-pathogen interactions 514 III. Mechanisms underlying continua in specificity and virulence 516 IV. Ecological consequences 519 V. Evolutionary patterns and processes 520 VI. Conclusions 524 Acknowledgements 525 References 525 Ecological, evolutionary and molecular models of interactions between plant hosts and microbial pathogens are largely based around a concept of tightly coupled interactions between species pairs. However, highly pathogenic and obligate associations between host and pathogen species represent only a fraction of the diversity encountered in natural and managed systems. Instead, many pathogens can infect a wide range of hosts, and most hosts are exposed to more than one pathogen species, often simultaneously. Furthermore, outcomes of pathogen infection vary widely because host plants vary in resistance and tolerance to infection, while pathogens are also variable in their ability to grow on or within hosts. Environmental heterogeneity further increases the potential for variation in plant host-pathogen interactions by influencing the degree and fitness consequences of infection. Here, we describe these continua of specificity and virulence inherent within plant host-pathogen interactions. Using this framework, we describe and contrast the genetic and environmental mechanisms that underlie this variation, outline consequences for epidemiology and community structure, explore likely ecological and evolutionary drivers, and highlight several key areas for future research.

Fleas are one of the most interesting and fascinating taxa of ectoparasites. All species in this relatively small order are obligatory haematophagous (blood-feeding) parasites of higher vertebrates. This book examines how functional, ecological and evolutionary patterns and processes of host-parasite relationships are realized in this particular system. As such it provides an in-depth case study of a host-parasite system, demonstrating how fleas can be used as a model taxon for testing ecological and evolutionary hypotheses. The book moves from basic descriptive aspects, to functional issues and finally to evolutionary explanations. It extracts several general principles that apply equally well to other host-parasite systems, so it appeals not only to flea biologists but also to 'mainstream' parasitologists and ecologists.

Oomycetes comprise a diverse group of organisms that morphologically resemble fungi but belong to the stramenopile lineage within the supergroup of chromalveolates. Recent studies have shown that plant pathogenic oomycetes have expanded gene families that are possibly linked to their pathogenic lifestyle. We analyzed the protein domain organization of 67 eukaryotic species including four oomycete and five fungal plant pathogens. We detected 246 expanded domains in fungal and oomycete plant pathogens. The analysis of genes differentially expressed during infection revealed a significant enrichment of genes encoding expanded domains as well as signal peptides linking a substantial part of these genes to pathogenicity. Overrepresentation and clustering of domain abundance profiles revealed domains that might have important roles in host-pathogen interactions but, as yet, have not been linked to pathogenicity. The number of distinct domain combinations (bigrams) in oomycetes was significantly higher than in fungi. We identified 773 oomycete-specific bigrams, with the majority composed of domains common to eukaryotes. The analyses enabled us to link domain content to biological processes such as host-pathogen interaction, nutrient uptake, or suppression and elicitation of plant immune responses. Taken together, this study represents a comprehensive overview of the domain repertoire of fungal and oomycete plant pathogens and points to novel features like domain expansion and species-specific bigram types that could, at least partially, explain why oomycetes are such remarkable plant pathogens.

Many bacterial plant pathogens require the type III secretion system (T3SS) and its effector proteins (T3SEs) to invade and extract nutrients from their hosts successfully. While the molecular function of this system is being studied intensively, we know comparatively little about the evolutionary and ecological pressures governing its fate over time, and even less about the detailed mechanisms underlying and driving complex T3SS-mediated coevolutionary dynamics. In this review we summarize our current understanding of how host-pathogen interactions evolve, with a particular focus on the T3SS of bacterial plant pathogens. We explore the evolutionary origins of the T3SS relative to the closely related flagellar system, and investigate the evolutionary pressures on this secretion and translocation apparatus. We examine the evolutionary forces acting on T3SEs, and compare the support for vertical descent with modification of these virulence-associated systems (pathoadaptation) vs horizontal gene transfer. We address the evolutionary origins of T3SEs from the perspective of both the evolutionary mechanisms that generate new effectors, and the mobile elements that may be the source of novel genetic material. Finally, we propose a number of questions raised by these studies, which may serve to guide our thinking about these complex processes.

Summary The hypersensitive defence response is found in all higher plants and is characterized by a rapid cell death at the point of pathogen ingress. It is usually associated with pathogen resistance, though, in specific situations, it may have other consequences such as pathogen susceptibility, growth retardation and, over evolutionary timescales, speciation. Due to the potentially severe costs of inappropriate activation, plants employ multiple mechanisms to suppress inappropriate activation of HR and to constrain it after activation. The ubiquity of this response among higher plants despite its costs suggests that it is an extremely effective component of the plant immune system.

Microbes have engaged in antagonistic associations with plants for hundreds of millions of years. Plants, in turn, have evolved diverse immune strategies to combat microbial pathogens. The conflicts between plants and pathogens result in everchanging coevolutionary cycles known as ‘Red Queen’ dynamics. These ancient and ongoing plant–pathogen interactions have shaped the evolution of both plant and pathogen genomes. With the recent explosion of plant genomescale data, comparative analyses provide novel insights into the coevolutionary dynamics of plants and pathogens. Here, we discuss the ancient associations between plants and microbes as well as the evolutionary principles underlying plant–pathogen interactions. We synthesize and review the current knowledge on the origin and evolution of key components of the plant immune system. We also highlight the importance of studying algae and nonflowering land plants in understanding the evolution of the plant immune system.

The immune system protects from infections primarily by detecting and eliminating the invading pathogens; however, the host organism can also protect itself from infectious diseases by reducing the negative impact of infections on host fitness. This ability to tolerate a pathogen's presence is a distinct host defense strategy, which has been largely overlooked in animal and human studies. Introduction of the notion of \"disease tolerance\" into the conceptual tool kit of immunology will expand our understanding of infectious diseases and host pathogen interactions. Analysis of disease tolerance mechanisms should provide new approaches for the treatment of infections and other diseases.

Plants require nitrogen (N) for growth, development and defence against abiotic and biotic stresses. The extensive use of artificial N fertilizers has played an important role in the Green Revolution. N assimilation can involve a reductase series ( NO3- → NO2- → NH4+ ) followed by transamination to form amino acids. Given its widespread use, the agricultural impact of N nutrition on disease development has been extensively examined. When a pathogen first comes into contact with a host, it is usually nutrient starved such that rapid assimilation of host nutrients is essential for successful pathogenesis. Equally, the host may reallocate its nutrients to defence responses or away from the site of attempted infection. Exogenous application of N fertilizer can, therefore, shift the balance in favour of the host or pathogen. In line with this, increasing N has been reported either to increase or to decrease plant resistance to pathogens, which reflects differences in the infection strategies of discrete pathogens. Beyond considering only N content, the use of NO3- or NH4+ fertilizers affects the outcome of plant-pathogen interactions. NO3- feeding augments hypersensitive response- (HR) mediated resistance, while ammonium nutrition can compromise defence. Metabolically, NO3- enhances production of polyamines such as spermine and spermidine, which are established defence signals, with NH4+ nutrition leading to increased γ-aminobutyric acid (GABA) levels which may be a nutrient source for the pathogen. Within the defensive N economy, the roles of nitric oxide must also be considered. This is mostly generated from NO2- by nitrate reductase and is elicited by both pathogen-associated microbial patterns and gene-for-gene-mediated defences. Nitric oxide (NO) production and associated defences are therefore NO3- dependent and are compromised by NH4+ . This review demonstrates how N content and form plays an essential role in defensive primary and secondary metabolism and NO-mediated events.

Many eukaryotes have obligate associations with microorganisms that are transmitted directly between generations. A model for heritable symbiosis is the association of aphids, a clade of sap-feeding insects, and Buchnera aphidicola , a gammaproteobacterium that colonized an aphid ancestor 150 million years ago and persists in almost all 5,000 aphid species. Symbiont acquisition enables evolutionary and ecological expansion; aphids are one of many insect groups that would not exist without heritable symbiosis. Receiving less attention are potential negative ramifications of symbiotic alliances. In the short run, symbionts impose metabolic costs. Over evolutionary time, hosts evolve dependence beyond the original benefits of the symbiosis. Symbiotic partners enter into an evolutionary spiral that leads to irreversible codependence and associated risks. Host adaptations to symbiosis (e.g., immune-system modification) may impose vulnerabilities. Symbiont genomes also continuously accumulate deleterious mutations, limiting their beneficial contributions and environmental tolerance. Finally, the fitness interests of obligate heritable symbionts are distinct from those of their hosts, leading to selfish tendencies. Thus, genes underlying the host–symbiont interface are predicted to follow a coevolutionary arms race, as observed for genes governing host–pathogen interactions. On the macroevolutionary scale, the rapid evolution of interacting symbiont and host genes is predicted to accelerate host speciation rates by generating genetic incompatibilities. However, degeneration of symbiont genomes may ultimately limit the ecological range of host species, potentially increasing extinction risk. Recent results for the aphid– Buchnera symbiosis and related systems illustrate that, whereas heritable symbiosis can expand ecological range and spur diversification, it also presents potential perils.

The major barrier to research and development of effective interventions for human noroviruses (HuNoVs) has been the lack of a robust and reproducible in vitro cultivation system. HuNoVs are the leading cause of gastroenteritis worldwide. We report the successful cultivation of multiple HuNoV strains in enterocytes in stem cell-derived, nontransformed human intestinal enteroid monolayer cultures. Bile, a critical factor of the intestinal milieu, is required for straindependent HuNoV replication. Lack of appropriate histoblood group antigen expression in intestinal cells restricts virus replication, and infectivity is abrogated by inactivation (e.g., irradiation, heating) and serum neutralization. This culture system recapitulates the human intestinal epithelium, permits human host-pathogen studies of previously noncultivatable pathogens, and allows the assessment of methods to prevent and treat HuNoV infections.