Annual Review of Phytopathology - Volume 51, 2013

Scale is an important but somewhat neglected subject in plant pathology. Scale serves as an abstract concept, providing a framework for organizing observations and theoretical models, and plays a functional role in the organization of ecological communities and physical processes. Rich methodological resources are available to plant pathologists interested in considering either or both aspects of scale in their research. We summarize important concepts in both areas of the literature, particularly as they apply to the spatial pattern of plant disease, and highlight some new results that emphasize the importance of scaling on the emergence of different types of probability distribution in empirical observation. We also highlight the important links between heterogeneity and scale, which are of central importance in plant disease epidemiology and the analysis of spatial pattern. We consider statistical approaches that are available, where actual physical scale is known, and for more conceptual research on hierarchies, where scale plays a more abstract role, particularly for field-based research. For the latter, we highlight methods that plant pathologists could consider to account for the effect of scale in the design of field studies.

Since the early 1980s, various strains of the gram-negative bacterial pathogen Pseudomonas syringae have been used as models for understanding plant-bacterial interactions. In 1991, a P. syringae pathovar tomato (Pst) strain, DC3000, was reported to infect not only its natural host tomato but also Arabidopsis in the laboratory, a finding that spurred intensive efforts in the subsequent two decades to characterize the molecular mechanisms by which this strain causes disease in plants. Genomic analysis shows that Pst DC3000 carries a large repertoire of potential virulence factors, including proteinaceous effectors that are secreted through the type III secretion system and a polyketide phytotoxin called coronatine, which structurally mimics the plant hormone jasmonate (JA). Study of Pst DC3000 pathogenesis has not only provided several conceptual advances in understanding how a bacterial pathogen employs type III effectors to suppress plant immune responses and promote disease susceptibility but has also facilitated the discovery of the immune function of stomata and key components of JA signaling in plants. The concepts derived from the study of Pst DC3000 pathogenesis may prove useful in understanding pathogenesis mechanisms of other plant pathogens.

Intercropping, the simultaneous cultivation of multiple crop species, has been used throughout history and remains common among farmers of small landholdings in the tropics. One benefit of this practice may be disease control. In phenomenological research comparing disease in monocrops and intercrops, primarily due to foliar fungi, intercropping reduced disease in 73% of more than 200 studies. Nematodes are the primary pathogen for which disease increases are reported, but variability in disease impacts among studies can be high for all types of diseases. The mechanisms by which intercrops affect disease dynamics include alteration of wind, rain, and vector dispersal; modification of microclimate, especially temperature and moisture; changes in host morphology and physiology; and direct pathogen inhibition. The effect of intercropping on host density is a factor underlying many of these mechanisms. By synthesizing our growing understanding of mechanisms and their interactions with phenomenological studies, we may develop a theoretical grounding that allows us to improve the application of intercropping for tropical smallholders and industrial farmers alike.

The ubiquitin-26S proteasome degradation system (UPS) in plants is involved in the signal transduction of many cellular processes, including host immune responses triggered by pathogen attack. Attacking pathogens produce effectors that are translocated into host cells, where they interfere with the host's defense signaling in very specific ways. Perhaps not surprising in view of the broad involvement of the host proteasome in plant immunity, certain bacterial effectors exploit or require the host UPS for their action, as currently best studied in Pseudomonas syringae. Intriguingly, some P. syringae strains also secrete the virulence factor syringolin A, which irreversibly inhibits the proteasome by a novel mechanism. Here, the role of the UPS in plant defense and its exploitation by effectors are summarized, and the biology, taxonomic distribution, and emerging implications for virulence strategies of syringolin A and similar compounds are discussed.

Programmed cell death (PCD) is essential for proper growth, development, and cellular homeostasis in all eukaryotes. The regulation of PCD is of central importance in plant-microbe interactions; notably, PCD and features associated with PCD are observed in many host resistance responses. Conversely, pathogen induction of inappropriate cell death in the host results in a susceptible phenotype and disease. Thus, the party in control of PCD has a distinct advantage in these battles. PCD processes appear to be of ancient origin, as indicated by the fact that many features of cell death strategy are conserved between animals and plants; however, some of the details of death execution differ. Mammalian core PCD genes, such as caspases, are not present in plant genomes. Similarly, pro- and antiapoptotic mammalian regulatory elements are absent in plants, but, remarkably, when expressed in plants, successfully impact plant PCD. Thus, subtle structural similarities independent of sequence homology appear to sustain operational equivalence. The vacuole is emerging as a key organelle in the modulation of plant PCD. Under different signals for cell death, the vacuole either fuses with the plasmalemma membrane or disintegrates. Moreover, the vacuole appears to play a key role in autophagy; evidence suggests a prosurvival function for autophagy, but other studies propose a prodeath phenotype. Here, we describe and discuss what we know and what we do not know about various PCD pathways and how the host integrates signals to activate salicylic acid and reactive oxygen pathways that orchestrate cell death. We suggest that it is not cell death as such but rather the processes leading to cell death that contribute to the outcome of a given plant-pathogen interaction.

Potato virus Y (PVY) is one of the oldest known plant viruses, and yet in the past 20 years it emerged in the United States as a relatively new and very serious problem in potato. The virus exists as a complex of strains that induce a wide variety of foliar and tuber symptoms in potato, leading to yield reduction and loss of tuber quality. PVY has displayed a distinct ability to evolve through accumulation of mutations and more rapidly through recombination between different strains, adapting to new potato cultivars across different environments. Factors behind PVY emergence as a serious potato threat are not clear at the moment, and here an attempt is made to analyze various properties of the virus and its interactions with potato resistance genes and with aphid vectors to explain this recent PVY spread in potato production areas. Recent advances in PVY resistance identification and mapping of corresponding genes are described. An updated classification is proposed for PVY strains that takes into account the most current information on virus molecular genetics, serology, and host reactivity.

Fungi and oomycetes that colonize living plant tissue form extensive interfaces with plant cells in which the cytoplasm of the microorganism is closely aligned with the host cytoplasm for an extended distance. In all cases, specialized biotrophic hyphae function to hijack host cellular processes across an interfacial zone consisting of a hyphal plasma membrane, a specialized interfacial matrix, and a plant-derived membrane. The interface is the site of active secretion by both players. This cross talk at the interface determines the winner in adversarial relationships and establishes the partnership in mutualistic relationships. Fungi and oomycetes secrete many specialized effector proteins for controlling the host, and they can stimulate remarkable cellular reorganization even in distant plant cells. Breakthroughs in live-cell imaging of fungal and oomycete encounter sites, including live-cell imaging of pathogens secreting fluorescently labeled effector proteins, have led to recent progress in understanding communication across the interface.