Disease induction by human microbial pathogens in plant-model systems: potential, problems and prospects

Item does not contain fulltextRelatively simple eukaryotic model organisms such as the genetic model weed plant Arabidopsis thaliana possess an innate immune system that shares important similarities with its mammalian counterpart. In fact, some human pathogens infect Arabidopsis and cause overt disease with human symptomology. In such cases, decisive elements of the plant's immune system are likely to be targeted by the same microbial factors that are necessary for causing disease in humans. These similarities can be exploited to identify elementary microbial pathogenicity factors and their corresponding targets in a green host. This circumvents important cost aspects that often frustrate studies in humans or animal models and, in addition, results in facile ethical clearance

Challenges in plant cellular pathway reconstruction based on gene expression profiling.

Item does not contain fulltextMicroarrays are used to profile transcriptional activity, providing global cell biology insight. Particularly for plants, interpretation of transcriptional profiles is challenging because many genes have unknown functions. Furthermore, many plant gene sequences do not have clear homologs in other model organisms. Fortunately, over the past five years, various tools that assist plant scientists have been developed. Here, we evaluate the currently available in silico tools for reconstruction of cellular (metabolic, biochemical and signal transduction) pathways based on plant gene expression datasets. Furthermore, we show how expression-profile comparison at the level of these various cellular pathways contributes to the postulation of novel hypotheses which, after experimental verification, can provide further insight into decisive elements that have roles in cellular processes

Soybean production in eastern and southern Africa and threat of yield loss due to soybean rust caused by Phakopsora pachyrhizi

Soybean is a major source of oil and proteins worldwide. The demand for soybean has increased in Africa, driven by the growing feed industry for poultry, aquaculture and home consumption in the form of processed milk, baked beans and for blending with maize and wheat flour. Soybean, in addition to being a major source of cooking oil, is also used in other industrial processes such as in the production of paints and candle wax. The demand for soybean in Africa so far outweighs the supply, hence the deficit is mainly covered through imports of soybean products such as soybean meal. The area under soybean production has increased in response to the growing demand, a trend that is expected to continue in the coming years. As the production area increases, diseases and insect pests, declining soil fertility and other abiotic factors pose a major challenge. Soybean rust disease, caused by the fungus Phakopsora pachyrhizi, presents one of the major threats to soybean production in Africa due to its rapid spread as a result of the ease by which its spores are dispersed by the wind. Disease control by introducing resistant soybean varieties has been difficult due to the presence of different populations of the fungus that vary in pathogenicity, virulence and genetic composition. Improved understanding of the dynamics of rust ecology, epidemiology and population genetics will enhance the effectiveness of targeted interventions that, in turn, will safeguard soybean productivity.</p

Molecular mechanisms of pathogenicity: how do pathogenic microorganisms develop cross-kingdom host jumps?

It is common knowledge that pathogenic viruses can change hosts, with avian influenza, the HIV, and the causal agent of variant Creutzfeldt-Jacob encephalitis as well-known examples. Less well known, however, is that host jumps also occur with more complex pathogenic microorganisms such as bacteria and fungi. In extreme cases, these host jumps even cross kingdom of life barriers. A number of requirements need to be met to enable a microorganism to cross such kingdom barriers. Potential cross-kingdom pathogenic microorganisms must be able to come into close and frequent contact with potential hosts, and must be able to overcome or evade host defences. Reproduction on, in, or near the new host will ensure the transmission or release of successful genotypes. An unexpectedly high number of cross-kingdom host shifts of bacterial and fungal pathogens are described in the literature. Interestingly, the molecular mechanisms underlying these shifts show commonalities. The evolution of pathogenicity towards novel hosts may be based on traits that were originally developed to ensure survival in the microorganism's original habitat, including former hosts.

Study of the role of antimicrobial glucosinolate-derived isothiocyanates in resistance of Arabidopsis to microbial pathogens.

Crude aqueous extracts from Arabidopsis leaves were subjected to chromatographic separations, after which the different fractions were monitored for antimicrobial activity using the fungus Neurospora crassa as a test organism. Two major fractions were obtained that appeared to have the same abundance in leaves from untreated plants versus leaves from plants challenge inoculated with the fungus Alternaria brassicicola. One of both major antimicrobial fractions was purified to homogeneity and identified by 1H nuclear magnetic resonance, gas chromatography/electron impact mass spectrometry, and gas chromatography/chemical ionization mass spectrometry as 4-methylsulphinylbutyl isothiocyanate (ITC). This compound has previously been described as a product of myrosinase-mediated breakdown of glucoraphanin, the predominant glucosinolate in Arabidopsis leaves. 4-Methylsulphinylbutyl ITC was found to be inhibitory to a wide range of fungi and bacteria, producing 50% growth inhibition in vitro at concentrations of 28 microM for the most sensitive organism tested (Pseudomonas syringae). A previously identified glucosinolate biosynthesis mutant, gsm1-1, was found to be largely deficient in either of the two major antimicrobial compounds, including 4-methylsulphinylbutyl ITC. The resistance of gsm1-1 was compared with that of wild-type plants after challenge with the fungi A. brassicicola, Plectosphaerella cucumerina, Botrytis cinerea, Fusarium oxysporum, or Peronospora parasitica, or the bacteria Erwinia carotovora or P. syringae. Of the tested pathogens, only F. oxysporum was found to be significantly more aggressive on gsm1-1 than on wild-type plants. Taken together, our data suggest that glucosinolate-derived antimicrobial ITCs can play a role in the protection of Arabidopsis against particular pathogens

Necrotroph Attacks on Plants: Wanton Destruction or Covert Extortion?

Necrotrophic pathogens cause major pre- and post-harvest diseases in numerous agronomic and horticultural crops inflicting significant economic losses. In contrast to biotrophs, obligate plant parasites that infect and feed on living cells, necrotrophs promote the destruction of host cells to feed on their contents. This difference underpins the divergent pathogenesis strategies and plant immune responses to biotrophic and necrotrophic infections. This chapter focuses on Arabidopsis immunity to necrotrophic pathogens. The strategies of infection, virulence and suppression of host defenses recruited by necrotrophs and the variation in host resistance mechanisms are highlighted. The multiplicity of intraspecific virulence factors and species diversity in necrotrophic organisms corresponds to variations in host resistance strategies. Resistance to host-specific necrotophs is monogenic whereas defense against broad host necrotrophs is complex, requiring the involvement of many genes and pathways for full resistance. Mechanisms and components of immunity such as the role of plant hormones, secondary metabolites, and pathogenesis proteins are presented. We will discuss the current state of knowledge of Arabidopsis immune responses to necrotrophic pathogens, the interactions of these responses with other defense pathways, and contemplate on the directions of future research

From Perception to Activation: The Molecular-Genetic and Biochemical Landscape of Disease Resistance Signaling in Plants

More than 60 years ago, H.H. Flor proposed the “Gene-for-Gene” hypothesis, which described the genetic relationship between host plants and pathogens. In the decades that followed Flor's seminal work, our understanding of the plant-pathogen interaction has evolved into a sophisticated model, detailing the molecular genetic and biochemical processes that control host-range, disease resistance signaling and susceptibility. The interaction between plants and microbes is an intimate exchange of signals that has evolved for millennia, resulting in the modification and adaptation of pathogen virulence strategies and host recognition elements. In total, plants have evolved mechanisms to combat the ever-changing landscape of biotic interactions bombarding their environment, while in parallel, plant pathogens have co-evolved mechanisms to sense and adapt to these changes. On average, the typical plant is susceptible to attack by dozens of microbial pathogens, yet in most cases, remains resistant to many of these challenges. The sum of research in our field has revealed that these interactions are regulated by multiple layers of intimately linked signaling networks. As an evolved model of Flor's initial observations, the current paradigm in host-pathogen interactions is that pathogen effector molecules, in large part, drive the recognition, activation and subsequent physiological responses in plants that give rise to resistance and susceptibility. In this Chapter, we will discuss our current understanding of the association between plants and microbial pathogens, detailing the pressures placed on both host and microbe to either maintain disease resistance, or induce susceptibility and disease. From recognition to transcriptional reprogramming, we will review current data and literature that has advanced the classical model of the Gene-for-Gene hypothesis to our current understanding of basal and effector triggered immunity