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Auswahl der wissenschaftlichen Literatur zum Thema „Host-Pathogen-Environment interaction“
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Zeitschriftenartikel zum Thema "Host-Pathogen-Environment interaction"
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Martinez-Martin, Nadia. „Technologies for Proteome-Wide Discovery of Extracellular Host-Pathogen Interactions“. Journal of Immunology Research 2017 (2017): 1–18. http://dx.doi.org/10.1155/2017/2197615.
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Pathogens have evolved unique mechanisms to breach the cell surface barrier and manipulate the host immune response to establish a productive infection. Proteins exposed to the extracellular environment, both cell surface-expressed receptors and secreted proteins, are essential targets for initial invasion and play key roles in pathogen recognition and subsequent immunoregulatory processes. The identification of the host and pathogen extracellular molecules and their interaction networks is fundamental to understanding tissue tropism and pathogenesis and to inform the development of therapeutic strategies. Nevertheless, the characterization of the proteins that function in the host-pathogen interface has been challenging, largely due to the technical challenges associated with detection of extracellular protein interactions. This review discusses available technologies for the high throughput study of extracellular protein interactions between pathogens and their hosts, with a focus on mammalian viruses and bacteria. Emerging work illustrates a rich landscape for extracellular host-pathogen interaction and points towards the evolution of multifunctional pathogen-encoded proteins. Further development and application of technologies for genome-wide identification of extracellular protein interactions will be important in deciphering functional host-pathogen interaction networks, laying the foundation for development of novel therapeutics.
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Chen, Melissa Y., Leah M. Fulton, Ivie Huang, Aileen Liman, Sarzana S. Hossain, Corri D. Hamilton, Siyu Song, Quentin Geissmann, Kayla C. King und Cara H. Haney. „Order among chaos: High throughput MYCroplanters can distinguish interacting drivers of host infection in a highly stochastic system“. PLOS Pathogens 21, Nr. 2 (11.02.2025): e1012894. https://doi.org/10.1371/journal.ppat.1012894.
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The likelihood that a host will be susceptible to infection is influenced by the interaction of diverse biotic and abiotic factors. As a result, substantial experimental replication and scalability are required to identify the contributions of and interactions between the host, the environment, and biotic factors such as the microbiome. For example, pathogen infection success is known to vary by host genotype, bacterial strain identity and dose, and pathogen dose. Elucidating the interactions between these factors in vivo has been challenging because testing combinations of these variables quickly becomes experimentally intractable. Here, we describe a novel high throughput plant growth system (MYCroplanters) to test how multiple host, non-pathogenic bacteria, and pathogen variables predict host health. Using an Arabidopsis-Pseudomonas host-microbe model, we found that host genotype and bacterial strain order of arrival predict host susceptibility to infection, but pathogen and non-pathogenic bacterial dose can overwhelm these effects. Host susceptibility to infection is therefore driven by complex interactions between multiple factors that can both mask and compensate for each other. However, regardless of host or inoculation conditions, the ratio of pathogen to non-pathogen emerged as a consistent correlate of disease. Our results demonstrate that high-throughput tools like MYCroplanters can isolate interacting drivers of host susceptibility to disease. Increasing the scale at which we can screen drivers of disease, such as microbiome community structure, will facilitate both disease predictions and treatments for medicine and agricultural applications.
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Burdon, J. J., und P. H. Thrall. „Resistance variation in natural plant populations“. Plant Protection Science 38, SI 1 - 6th Conf EFPP 2002 (01.01.2002): S145—S150. http://dx.doi.org/10.17221/10342-pps.
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The general outcomes of long-term trajectories of coevolutionary interactions between specific hosts and pathogens are<br />set by the interaction of their life histories. However, within those outcomes the speed of co-evolutionary responses and<br />the extent of their expression in the resistance/virulence structure of wild plant and pathogen populations respectively,<br />are highly variable characters changing from place-to-place and time-to-time as a result of the interaction of host and<br />pathogen with the physical environment. As a consequence, understanding of the role of diseases in the evolution of their<br />hosts requires approaches that simultaneously deal with host and pathogen structures over multiple populations within a<br />metapopulation framework.
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Wroth, J. M. „Variation in pathogenicity among and within Mycosphaerella pinodes populations collected from field pea in Australia“. Canadian Journal of Botany 76, Nr. 11 (01.11.1998): 1955–66. http://dx.doi.org/10.1139/b98-164.
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Ninety-nine single ascospore isolates of Mycosphaerella pinodes (Berk. & Blox.) Vestergr. from widely separated locations in southern Australia varied greatly in their ability to cause disease in leaves and stems of 10 host genotypes when assayed at two inoculum pressures. There were highly significant differences between the infection pressures, isolates, and host genotypes that accounted for most of the variance. A small proportion of the variance included a highly significant host genotype beta isolate interactions in leaves and stems and a highly significant host genotype beta isolate beta environment interaction in leaves. The continuous variation in disease responses among isolates precluded classification into distinct pathotypes. A cluster analysis of the data revealed that many isolates were closely related irrespective of the host cultivar or location from which they were collected. The relationship between mean host resistance and the variation among isolates was assessed, and it was concluded that increasing host resistance was unlikely to increase variation in the pathogen population; therefore, resistance should be relatively stable.Key words: Ascochyta blight, Pisum sativum, host-pathogen interaction, cluster analysis.
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Blaustein, Andrew R., Stephanie S. Gervasi, Pieter T. J. Johnson, Jason T. Hoverman, Lisa K. Belden, Paul W. Bradley und Gisselle Y. Xie. „Ecophysiology meets conservation: understanding the role of disease in amphibian population declines“. Philosophical Transactions of the Royal Society B: Biological Sciences 367, Nr. 1596 (19.06.2012): 1688–707. http://dx.doi.org/10.1098/rstb.2012.0011.
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Infectious diseases are intimately associated with the dynamics of biodiversity. However, the role that infectious disease plays within ecological communities is complex. The complex effects of infectious disease at the scale of communities and ecosystems are driven by the interaction between host and pathogen. Whether or not a given host–pathogen interaction results in progression from infection to disease is largely dependent on the physiological characteristics of the host within the context of the external environment. Here, we highlight the importance of understanding the outcome of infection and disease in the context of host ecophysiology using amphibians as a model system. Amphibians are ideal for such a discussion because many of their populations are experiencing declines and extinctions, with disease as an important factor implicated in many declines and extinctions. Exposure to pathogens and the host's responses to infection can be influenced by many factors related to physiology such as host life history, immunology, endocrinology, resource acquisition, behaviour and changing climates. In our review, we discuss the relationship between disease and biodiversity. We highlight the dynamics of three amphibian host–pathogen systems that induce different effects on hosts and life stages and illustrate the complexity of amphibian–host–parasite systems. We then review links between environmental stress, endocrine–immune interactions, disease and climate change.
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Haley, Kathryn P., und Jennifer A. Gaddy. „Helicobacter pylori: Genomic Insight into the Host-Pathogen Interaction“. International Journal of Genomics 2015 (2015): 1–8. http://dx.doi.org/10.1155/2015/386905.
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The advent of genomic analyses has revolutionized the study of human health. Infectious disease research in particular has experienced an explosion of bacterial genomic, transcriptomic, and proteomic data complementing the phenotypic methods employed in traditional bacteriology. Together, these techniques have revealed novel virulence determinants in numerous pathogens and have provided information for potential chemotherapeutics. The bacterial pathogen,Helicobacter pylori, has been recognized as a class 1 carcinogen and contributes to chronic inflammation within the gastric niche. Genomic analyses have uncovered remarkable coevolution between the human host andH. pylori. Perturbation of this coevolution results in dysregulation of the host-pathogen interaction, leading to oncogenic effects. This review discusses the relationship ofH. pyloriwith the human host and environment and the contribution of each of these factors to disease progression, with an emphasis on features that have been illuminated by genomic tools.
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Gaylord, Elizabeth A., Hau Lam Choy und Tamara L. Doering. „Dangerous Liaisons: Interactions of Cryptococcus neoformans with Host Phagocytes“. Pathogens 9, Nr. 11 (27.10.2020): 891. http://dx.doi.org/10.3390/pathogens9110891.
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Cryptococcus neoformans is an opportunistic fungal pathogen and a leading cause of death in immunocompromised individuals. The interactions of this yeast with host phagocytes are critical to disease outcome, and C. neoformans is equipped with an array of factors to modulate these processes. Cryptococcal infection begins with the deposition of infectious particles into the lungs, where the fungal cells deploy various antiphagocytic factors to resist internalization by host cells. If the cryptococci are still engulfed, they can survive and proliferate within host cells by modulating the phagolysosome environment in which they reside. Lastly, cryptococcal cells may escape from phagocytes by host cell lysis, nonlytic exocytosis, or lateral cell-to-cell transfer. The interactions between C. neoformans and host phagocytes also influence the dissemination of this pathogen to the brain, where it may cross the blood-brain barrier and cause an often-fatal meningoencephalitis. In this review, we highlight key cryptococcal factors involved in various stages of cryptococcal-host interaction and pathogenesis.
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Tung, Pham X., Eufemio T. Rasco, Peter Vander Zaag und Peter Schmiediche. „Resistance to Pseudomonas solanacearum in the potato: II. Aspects of host-pathogen-environment interaction“. Euphytica 45, Nr. 3 (Februar 1990): 211–15. http://dx.doi.org/10.1007/bf00032988.
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Tamir-Ariel, Dafna, Naama Navon und Saul Burdman. „Identification of Genes in Xanthomonas campestris pv. vesicatoria Induced during Its Interaction with Tomato“. Journal of Bacteriology 189, Nr. 17 (15.06.2007): 6359–71. http://dx.doi.org/10.1128/jb.00320-07.
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ABSTRACT Xanthomonas campestris pv. vesicatoria is the causal agent of bacterial spot disease of tomato and pepper. The disease process is interactive and very intricate and involves a plethora of genes in the pathogen and in the host. In the pathogen, different genes are activated in response to the changing environment to enable it to survive, adapt, evade host defenses, propagate, and damage the host. To understand the disease process, it is imperative to broaden our understanding of the gene machinery that participates in it, and the most reliable way is to identify these genes in vivo. Here, we have adapted a recombinase-based in vivo expression technology (RIVET) to study the genes activated in X. campestris pv. vesicatoria during its interaction with one of its hosts, tomato. This is the first study that demonstrates the feasibility of this approach for identifying in vivo induced genes in a plant pathogen. RIVET revealed 61 unique X. campestris pv. vesicatoria genes or operons that delineate a picture of the different processes involved in the pathogen-host interaction. To further explore the role of some of these genes, we generated knockout mutants for 13 genes and characterized their ability to grow in planta and to cause disease symptoms. This analysis revealed several genes that may be important for the interaction of the pathogen with its host, including a citH homologue gene, encoding a citrate transporter, which was shown to be required for wild-type levels of virulence.
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Mehta, Sahil, Amrita Chakraborty, Amit Roy, Indrakant K. Singh und Archana Singh. „Fight Hard or Die Trying: Current Status of Lipid Signaling during Plant–Pathogen Interaction“. Plants 10, Nr. 6 (30.05.2021): 1098. http://dx.doi.org/10.3390/plants10061098.
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Plant diseases pose a substantial threat to food availability, accessibility, and security as they account for economic losses of nearly $300 billion on a global scale. Although various strategies exist to reduce the impact of diseases, they can introduce harmful chemicals to the food chain and have an impact on the environment. Therefore, it is necessary to understand and exploit the plants’ immune systems to control the spread of pathogens and enable sustainable agriculture. Recently, growing pieces of evidence suggest a functional myriad of lipids to be involved in providing structural integrity, intracellular and extracellular signal transduction mediators to substantial cross-kingdom cell signaling at the host–pathogen interface. Furthermore, some pathogens recognize or exchange plant lipid-derived signals to identify an appropriate host or development, whereas others activate defense-related gene expression. Typically, the membrane serves as a reservoir of lipids. The set of lipids involved in plant–pathogen interaction includes fatty acids, oxylipins, phospholipids, glycolipids, glycerolipids, sphingolipids, and sterols. Overall, lipid signals influence plant–pathogen interactions at various levels ranging from the communication of virulence factors to the activation and implementation of host plant immune defenses. The current review aims to summarize the progress made in recent years regarding the involvement of lipids in plant–pathogen interaction and their crucial role in signal transduction.
Dissertationen zum Thema "Host-Pathogen-Environment interaction"
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Duperret, Léo. „Caractérisation des mécanismes moléculaires de la permissivité au Syndrome de Mortalité de l'Huître du Pacifique (POMS) sous influence de la température et du régime alimentaire“. Electronic Thesis or Diss., Perpignan, 2024. http://www.theses.fr/2024PERP0042.
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Les systèmes de production alimentaire ont dû répondre ces dernières décennies à une demande alimentaire croissante générée par l'augmentation exponentielle de la population humaine. Ceci a mené à une intensification des cultures, des élevages et de la pêche au détriment des stocks et de la santé de notre planète. Pour le milieu marin, l'intensification de la pêche a conduit à l'amenuisement de certains stocks et à la mise en place de quotas. Cette diminution des ressources halieutiques a conduit au développement de l'aquaculture, une pratique d'élevage de la ressource bleue. Cependant, avec la surproduction et les changements globaux nous assistons à une recrudescence des épizooties depuis 1970, surtout chez les orgnaismes ectothermes. La maladie du POMS (Pacific Oyster Mortality Syndrome) en est une parfaite illustration puisqu'elle est responsable, chaque année, d'importants épisodes de mortalités chez les juvéniles de l'espèce d'huître Magallana gigas dans l'ensemble des pays producteurs. Maladie polymicrobienne apparue en 2008 en France, sa pathogénicité dépend de multiples facteurs dont la température (entre 16 et 24°C sur les côtes françaises) et la disponibilité en ressources nutritives. Alors que de nombreuses recherches ont permis de caractériser la pathogénèse et d'identifier les différents facteurs influençant le développement de cette maladie, les mécanismes moléculaires responsables des variations de permissivité en fonction de ces facteurs demeurent encore largement inconnus. Cette thèse s'inscrit donc dans cet objectif. Par un design expérimental rigoureux, une approche holistique et une analyse comparative intégrative à différentes échelles dans des conditions permissives et non-permissives à la maladie, nous avons pu identifier les mécanismes moléculaires sous-jacents à la permissivité liée à la température et à la ressource alimentaire. Ces résultats permettent de mieux comprendre la complexité de cette interaction hôte-pathogène-environnement et permettront à terme d'implémenter des modèles prédictifs du risque épidémiologiqueOver the past decades, food production systems have had to meet the growing demand for food driven by the exponential increase in the global human population. This demand has led to intensified agriculture, livestock farming, and fishing practices, often at the expense of natural resources and planetary health. In the marine environment, intensified fishing has resulted in the depletion of certain stocks and the implementation of fishing quotas. The decline in marine resources has prompted the development of aquaculture, a practice for farming blue resources. However, with overproduction and global environmental changes, we have witnessed an upsurge in epizootics since 1970, particularly among ectothermic organisms. The Pacific Oyster Mortality Syndrome (POMS) is a prime example, responsible for significant annual mortality episodes in juvenile oysters of the species Magallana gigas across major producing countries. Emerging in 2008 in France, this polymicrobial disease is influenced by several factors, including temperature (between 16°C and 24°C along the French coasts) and the availability of nutritional resources. Although extensive research has helped characterize its pathogenesis and identify the various factors influencing the development of the disease, the molecular mechanisms underlying variations in permissiveness according to these factors remain largely unknown. This thesis addresses this objective. Through a rigorous experimental design, a holistic approach, and an integrative comparative analysis at multiple scales under permissive and non-permissive conditions for the disease, we identified the molecular mechanisms underlying permissiveness related to temperature and nutritional resources. These findings enhance our understanding of the complexity of host-pathogen-environment interactions and will ultimately contribute to the development of predictive models for epidemiological risk
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Schmertmann, Laura. „The Cryptococcus gattii species complex in koalas: host-pathogen-environment interactions and molecular epidemiology“. Thesis, The University of Sydney, 2019. http://hdl.handle.net/2123/20769.
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The Cryptococcus gattii species complex comprises some of the aetiological agents of cryptococcosis, a severe fungal disease that affects a wide variety of hosts and is acquired from the environment by inhalation. Koalas (Phascolarctos cinereus) appear to be particularly susceptible to cryptococcosis. In Australia, eucalypt tree hollows are the classic ecological niche for C. gattii molecular type VGI and therefore are also a potential source of infection. Aspects of the tree hollow microenvironment that may allow for the growth and dispersal of C. gattii VGI remain poorly understood. The C. gattii species complex has been associated with outbreaks and case clusters, and animals are often considered useful sentinels for the disease in these scenarios. The prevalence of cryptococcosis in Australian wildlife remains unknown. Given the koala’s propensity towards developing cryptococcosis, and its regular contact with a common ecological niche for the C. gattii species complex (eucalypts), it is an ideal sentinel species. The host-pathogen-environment interactions of cryptococcosis caused by the C. gattii species complex, particularly progression from exposure to colonisation of the respiratory mucosa to eventual tissue invasion, remain poorly understood. This thesis uses amplicon-based next generation sequencing to characterise the fungal microbiome of Australian tree hollows, focusing on the role that the C. gattii species complex may play in this microenvironment. The prevalence of cryptococcosis in a population of free-ranging koalas is systematically characterised, while the pathogenesis, treatment and diagnosis of the disease in this host species are also explored. Finally, fine-scale molecular epidemiology tools (multi-locus sequence typing and whole genome sequencing) are used to determine sources of infection and examine disease caused by the C. gattii species complex in Australia, using primarily the koala as a model for naturally-occurring cryptococcosis.
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HÖNIG, Václav. „Spatial Distribution of Tick-Borne Pathogens as a Consequence of Vector-Host-Pathogen Interactions with Environment“. Doctoral thesis, 2015. http://www.nusl.cz/ntk/nusl-201343.
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The proposed thesis contributes to the basic knowledge in tick (Ixodes ricinus) and tick-borne pathogens (Borrelia burgdorferi sensu lato, tick-borne encephalitis virus) ecology in particular studying the spatial distribution, host associations and its causes and consequences in Central European habitats.
Bücher zum Thema "Host-Pathogen-Environment interaction"
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Roche, Benjamin, Hélène Broutin und Frédéric Simard, Hrsg. Ecology and Evolution of Infectious Diseases. Oxford University Press, 2018. http://dx.doi.org/10.1093/oso/9780198789833.001.0001.
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During the last thirty years, the ecology and evolution of infectious diseases has been studied extensively. Understanding how pathogens are transmitted in time and space, how they are evolving according to different selective pressures, and how the environment can influence their transmission, has paved the way for new approaches to the study of host/pathogen interactions. At the same time, pathogen control in low-income countries (LIC) has tended to remain largely inspired and informed by classical epidemiology, where the objective is to treat as many people as possible, despite recent findings in ecology and evolutionary biology suggesting new opportunities for improved disease control in the context of limited economic resources. The need to integrate the scientific developments in ecology and evolution of infectious diseases with public health strategy in low-income countries is clearly as important today as it has ever been. In this book, the authors provide an up to date, authoritative, and challenging review of the ecology and evolution of infectious diseases focusing on low-income countries for effective public health applications and outcomes. Accessible to students and researchers working on evolutionary ecology of infectious diseases and public health scientists working on their control in low-income countries, this book combines chapters exposing fundamental concepts in evolutionary ecology with others exploring the most recent advances in the field as well as highlighting how they can provide new innovative approach on the field. This work is concluded by an integrative chapter signed by all the authors highlighting the key missing points to improve this connection between evolutionary ecology and public health in low-income countries.
Buchteile zum Thema "Host-Pathogen-Environment interaction"
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Prabhu, Ashish A., und V. Venkatadasu. „Systems and Synthetic Biology Approach to Understand the Importance of Host-Pathogen Interaction“. In Microbial Interventions in Agriculture and Environment, 433–46. Singapore: Springer Singapore, 2019. http://dx.doi.org/10.1007/978-981-32-9084-6_19.
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Ulrich, Danielle E. M., Steve Voelker, J. Renée Brooks und Frederick C. Meinzer. „Insect and Pathogen Influences on Tree-Ring Stable Isotopes“. In Stable Isotopes in Tree Rings, 711–36. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-92698-4_25.
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AbstractUnderstanding long-term insect and pathogen effects on host tree physiology can help forest managers respond to insect and pathogen outbreaks, and understand when insect and pathogen effects on tree physiology will be exacerbated by climate change. Leaf-level physiological processes modify the carbon (C) and oxygen (O) stable isotopic composition of elements taken up from the environment, and these modifications are recorded in tree-rings (see Chaps. 10.1007/978-3-030-92698-4_9, 10.1007/978-3-030-92698-4_10, 10.1007/978-3-030-92698-4_16 and 10.1007/978-3-030-92698-4_17). Therefore, tree-ring stable isotopes are affected by both the tree’s environment and the tree’s physiological responses to the environment, including insects and pathogens. Tree-ring stable isotopes provide unique insights into the long-term effects of insects and pathogens on host tree physiology. However, insect and pathogen impacts on tree-ring stable isotopes are often overlooked, yet can substantially alter interpretations of tree-ring stable isotopes for reconstructions of climate and physiology. In this chapter, we discuss (1) the effects of insects(defoliators, wood-boring, leaf-feeding), pests (parasitic plants), and pathogens(root and foliar fungi) on hostphysiology (growth, hormonal regulation, gas exchange, water relations, and carbon and nutrient use) as they relate to signals possibly recorded by C and O stable isotopes in tree-rings, (2) how tree-ring stable isotopes reveal insect and pathogen impacts and the interacting effects of pathogens and climate on hostphysiology, and (3) the importance of considering insect and pathogen impacts for interpreting tree-ring stable isotopes to reconstruct past climate or physiology.
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Prusky, Dov, Shiri Barad, Neta Luria und Dana Ment. „pH Modulation of Host Environment, a Mechanism Modulating Fungal Attack in Postharvest Pathogen Interactions“. In Post-harvest Pathology, 11–25. Cham: Springer International Publishing, 2014. http://dx.doi.org/10.1007/978-3-319-07701-7_2.
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Aly, Sharif S., und Sarah M. Depenbrock. „Preventing bacterial diseases in dairy cattle“. In Improving dairy herd health Improving, 395–456. Burleigh Dodds Science Publishing, 2021. http://dx.doi.org/10.19103/as.2020.0086.16.
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A paradigm shift in the management of bacterial diseases of food animals is needed; a shift from pharmacologic interventions to disease risk identification and mitigation. The interaction between disease and its risk factors follows the disease triangle, a conceptual model that incorporates host, pathogen, and environmental factors as a tool to understand different aspects that influence disease. A sustainable approach to bacterial disease mitigation in production settings includes a comprehensive assessment of host, pathogen, and environmental factors of disease to build a prevention platform for multiple syndromes of bacterial disease in cattle. Using bovine respiratory disease as a model, the current chapter will focus on the state of the art of disease prevention in dairy cattle, and investigations into interactions between the host, environment and pathogen which can provide robust information on which to build a prevention platform for multiple syndromes of bacterial disease in cattle.
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Bateman, Kelly S., Stephen W. Feist, John P. Bignell, David Bass und Grant D. Stentiford. „Marine pathogen diversity and disease outcomes“. In Marine Disease Ecology, 3–44. Oxford University Press, 2020. http://dx.doi.org/10.1093/oso/9780198821632.003.0001.
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This chapter provides an introduction to important marine pathogens, providing an overview of the diversity of pathogen types and how they affect different hosts in the marine environment. The chapter focuses on wild and cultured species and highlights that single infections are relatively rare, with co- and secondary infections being commonplace. The authors highlight the importance of understanding “normal” host tissue structure prior to interpreting pathological changes and outline the role of histology to assess pathogenicity of emerging diseases, linking presence of individual pathogens and co-infections with degree of host response. Fact sheets focus on the pathology (i.e., interaction of a specific pathogen group with the host cell/system) with high-quality histology and TEM images, emphasizing tissue changes caused by pathogens, and point the reader to presumptive diagnosis via histology while highlighting the need for confirmatory testing via other means. The pathobiome concept is introduced and explained, and the utility for predicting outcomes at the individual and population levels discussed.
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Marquis, Jean-Francois, John R. Forbes, Francois Canonne-Hergaux, Cynthia Horth und Philippe Gros. „Metal Transport Genes“. In Genetic Susceptibility to Infectious Diseases, 175–89. Oxford University PressNew York, NY, 2008. http://dx.doi.org/10.1093/oso/9780195174908.003.0013.
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Abstract Susceptibility to infections, with respect to initial onset, progression, and ultimate outcome of disease, is influenced by a number of factors, including pathogenencoded virulence determinants, the genetic makeup of the host, and environmental factors that can modulate the expression of both. The laboratory mouse has been a valuable model for the genetic analysis of host susceptibility determinants and pathogen-encoded virulence factors. The discovery of a mutation in a macrophage-specific metal transporter that causes susceptibility to infection by several unrelated intracellular pathogens has suggested that metal deprivation is a critical mechanism by which macrophages restrict replication of intracellular pathogens. Likewise, the observation that pathogens possess a number of metal acquisition systems, some of which are essential for virulence in vivo, has confirmed the critical importance of divalent metals in the outcome of host–pathogen interaction. Metals may be required for the basic metabolic activity necessary for expression of intracellular survival strategies, including the modulation of phagosome maturation, and=or may be required for the activity of microbial enzymes essential for detoxification of the phagosomal environment. This review discusses two families of mammalian metal transporters expressed in macrophages, Nramp (Slc11a1, Slc11a2) and ferroportin (Slc40a1), and the possible roles these proteins play in the antimicrobial properties of these cells. Recent studies characterizing the biochemical content of bacterial phagosomes formed in macrophages, and the transcriptional responses of bacteria exposed to this environment are also reviewed.
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Singh, Joginder, Joydeep Dutta und Ravi Kant Pathak. „Antibacterial Peptides: Potential Therapeutic Agent“. In Recent Trends and The Future of Antimicrobial Agents - Part I, 61–92. BENTHAM SCIENCE PUBLISHERS, 2023. http://dx.doi.org/10.2174/9789815079609123010006.
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With the changing environment, microbial pathogens continuously develop antibiotic resistance (AR). As a response to this host-pathogen interaction, host organisms sometimes develop a strategy to stay ahead of the AR developed by pathogens. These molecules are small peptides known as antimicrobial peptides (AMPs). These peptides are short in length, specific in structure and thus have a unique mechanism of action. The uniqueness and specificity in the mechanism come due to the positively charged amino acids which are responsible for initial interaction among AMPs and the negatively charged membrane of the pathogenic cell. Microbes do not develop much ABR against AMPs because of the absence of epitopic regions on AMPs. This property makes AMPs the new therapeutic strategy against microbes. Here, we present a review of the AMPs, their sequence, structure, classification, mechanism of action and the computational strategy developed so far to identify new and improved AMPs that can be used as therapeutic agents.
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Afifi, Mohammed A., Mohammed W. Al-Rabia und Deema I. Fallatah. „Animal Modeling of Infectious Diseases“. In Animal Models In Experimental Medicine, 20–54. BENTHAM SCIENCE PUBLISHERS, 2024. http://dx.doi.org/10.2174/9789815196382124010005.
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Animal models have been, and continue to be, viable tools for investigating crucial scientific issues related to the pathogenesis of infectious diseases and serve as living platforms for testing novel therapeutics and/or vaccines. The use of animal models in studying infectious diseases is not only founded on the substantially shared biology of most mammals but also on the fact that many human infections are zoonotic, affecting a range of animal species. However, it is noticeable that the results retrieved from animal studies are not always reproducible in studies conducted on humans. The reliability of correlating data from animal models and translating them to human disease succeeds only in well-designed models where their relevance to the investigated human disease is well recognized. Preferable animal models respond similarly to the infectious agent as in humans, where the host’s interaction with the pathogen creates the same immunological and molecular environment. Several animal models have been designed to investigate the different aspects of the infectious process, such as biology, immunology, and pathogenesis. The murine model has been chosen for most studies investigating infectious diseases. Despite the limitations of the current animal models, remarkable progress has been achieved using these models, including a better understanding of host immune responses to infection, microbiome–pathogen interactions, the molecular mechanisms underlying tissue damage as well as validation of novel therapeutics and vaccine development.
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Owen, Jennifer C., James S. Adelman und Amberleigh E. Henschen. „The Nature of Host–Pathogen Interactions“. In Infectious Disease Ecology of Wild Birds, 7–28. Oxford University Press, 2021. http://dx.doi.org/10.1093/oso/9780198746249.003.0002.
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The dynamics of infectious disease are driven by the fundamental processes that mediate host–pathogen interactions. A basic understanding of the mechanisms underlying these interactions is essential for disease ecologists regardless of their scale of inquiry. This chapter covers the terms and concepts commonly used in ecological studies of infectious disease across levels of organization and scales of inquiry, from the individual host organism to host populations and multispecies communities. When applicable, aspects that are unique to birds and their biology are highlighted. The between-host processes discussed in the beginning of the chapter arise from the within-host processes between the pathogen and the host’s immune system. These processes are then used as a framework to introduce the basics of epidemiological modeling and the population-level disease dynamics. The chapter is not meant to be exhaustive but, instead, to provide a common foundation for readers approaching this topic from unique backgrounds. Given the transdisciplinary nature of avian infectious disease ecology, many of the terms used have multiple meanings assigned to them that are taxon- or discipline-specific. Such variation in key terminology is, in large part, a consequence of the transdisciplinary and multiscaled approaches inherent in studying host–pathogen–vector–environment interactions.
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F. Ramos, Rodrigo, Lisiane Sobucki, Estéfany Pawlowski, Janaina S. Sarzi, Jessica E. Rabuske, Lucas G. Savian, Tiago E. Kaspary und Cristiano Bellé. „Perspective Chapter: Microorganisms and Their Relationship with Tree Health“. In Current and Emerging Challenges in the Diseases of Trees [Working Title]. IntechOpen, 2023. http://dx.doi.org/10.5772/intechopen.110461.
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The health of plants depends on numerous environmental factors. All plants, including trees, live in close relationship with microorganisms. Plants harbor microbial communities in above- and below-ground tissues, where plant-associated microbial communities are influenced by environmental conditions and host genotype. The microbiome of trees is composed of mutualistic, commensal, and pathogenic microorganisms. Mutualistic microorganisms can help trees obtain nutrients (e.g., phosphorus and nitrogen) and defend against plant pathogens. Ecological interactions between different microbial groups directly influence host health, and endophytic microorganisms can inhibit pathogen growth or induce the expression of genes related to tree defense against these adverse organisms. Hence, understanding host-microbiome-environment interactions are crucial for modulating tree health.
Berichte der Organisationen zum Thema "Host-Pathogen-Environment interaction"
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Horwitz, Benjamin A., und Barbara Gillian Turgeon. Fungal Iron Acquisition, Oxidative Stress and Virulence in the Cochliobolus-maize Interaction. United States Department of Agriculture, März 2012. http://dx.doi.org/10.32747/2012.7709885.bard.
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Our project focused on genes for high affinity iron acquisition in Cochliobolus heterostrophus, a necrotrophic pathogen of maize, and their intertwined relationship to oxidative stress status and virulence of the fungus on the host. An intriguing question was why mutants lacking the nonribosomal peptide synthetase (NRPS) gene (NPS6) responsible for synthesis of the extracellular siderophore, coprogen, are sensitive to oxidative stress. Our overall objective was to understand the mechanistic connection between iron stress and oxidative stress as related to virulence of a plant pathogen to its host. The first objective was to examine the interface where small molecule peptide and reactive oxygen species (ROS) mechanisms overlap. The second objective was to determine if the molecular explanation for common function is common signal transduction pathways. These pathways, built around sensor kinases, response regulators, and transcription factors may link sequestering of iron, production of antioxidants, resistance to oxidative stress, and virulence. We tested these hypotheses by genetic manipulation of the pathogen, virulence assays on the host plant, and by following the expression of key fungal genes. An addition to the original program, made in the first year, was to develop, for fungi, a genetically encoded indicator of redox state based on the commercially available Gfp-based probe pHyper, designed for animal cell biology. We implemented several tools including a genetically encoded indicator of redox state, a procedure to grow iron-depleted plants, and constructed a number of new mutants in regulatory genes. Lack of the major Fe acquisition pathways results in an almost completely avirulent phenotype, showing how critical Fe acquisition is for the pathogen to cause disease. Mutants in conserved signaling pathways have normal ability to regulate NPS6 in response to Fe levels, as do mutants in Lae1 and Vel1, two master regulators of gene expression. Vel1 mutants are sensitive to oxidative stress, and the reason may be underexpression of a catalase gene. In nps6 mutants, CAT3 is also underexpressed, perhaps explaining the sensitivity to oxidative stress. We constructed a deletion mutant for the Fe sensor-regulator SreA and found that it is required for down regulation of NPS6 under Fe-replete conditions. Lack of SreA, though, did not make the fungus over-sensitive to ROS, though the mutant had a slow growth rate. This suggests that overproduction of siderophore under Fe-replete conditions is not very damaging. On the other hand, increasing Fe levels protected nps6 mutants from inhibition by ROS, implying that Fe-catalyzed Fenton reactions are not the main factor in its sensitivity to ROS. We have made some progress in understanding why siderophore mutants are sensitive to oxidative stress, and in doing so, defined some novel regulatory relationships. Catalase genes, which are not directly related to siderophore biosynthesis, are underexpressed in nps6 mutants, suggesting that the siderophore product (with or without bound Fe) may act as a signal. Siderophores, therefore, could be a target for intervention in the field, either by supplying an incorrect signal or blocking a signal normally provided during infection. We already know that nps6 mutants cause smaller lesions and have difficulty establishing invasive growth in the host. Lae1 and Vel1 are the first factors shown to regulate both super virulence conferred by T-toxin, and basic pathogenicity, due to unknown factors. The mutants are also altered in oxidative stress responses, key to success in the infection court, asexual and sexual development, essential for fungal dissemination in the field, aerial hyphal growth, and pigment biosynthesis, essential for survival in the field. Mutants in genes encoding NADPH oxidase (Nox) are compromised in development and virulence. Indeed the triple mutant, which should lack all Nox activity, was nearly avirulent. Again, gene expression experiments provided us with initial evidence that superoxide produced by the fungus may be most important as a signal. Blocking oxidant production by the pathogen may be a way to protect the plant host, in interactions with necrotrophs such as C. heterostrophus which seem to thrive in an oxidant environment.
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Eldar, Avigdor, und Donald L. Evans. Streptococcus iniae Infections in Trout and Tilapia: Host-Pathogen Interactions, the Immune Response Toward the Pathogen and Vaccine Formulation. United States Department of Agriculture, Dezember 2000. http://dx.doi.org/10.32747/2000.7575286.bard.
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In Israel and in the U.S., Streptococcus iniae is responsible for considerable losses in various fish species. Poor understanding of its virulence factors and limited know-how-to of vaccine formulation and administration are the main reasons for the limited efficacy of vaccines. Our strategy was that in order to Improve control measures, both aspects should be equally addressed. Our proposal included the following objectives: (i) construction of host-pathogen interaction models; (ii) characterization of virulence factors and immunodominant antigens, with assessment of their relative importance in terms of protection and (iii) genetic identification of virulence factors and genes, with evaluation of the protective effect of recombinant proteins. We have shown that two different serotypes are involved. Their capsular polysaccharides (CPS) were characterized, and proved to play an important role in immune evasion and in other consequences of the infection. This is an innovative finding in fish bacteriology and resembles what, in other fields, has become apparent in the recent years: S. iniae alters surface antigens. By so doing, the pathogen escapes immune destruction. Immunological assays (agar-gel immunodiffusion and antibody titers) confirmed that only limited cross recognition between the two types occurs and that capsular polysaccharides are immunodominant. Vaccination with purified CPS (as an acellular vaccine) results in protection. In vitro and ex-vivo models have allowed us to unravel additional insights of the host-pathogen interactions. S. iniae 173 (type II) produced DNA fragmentation of TMB-8 cells characteristic of cellular necrosis; the same isolate also prevented the development of apoptosis in NCC. This was determined by finding reduced expression of phosphotidylserine (PS) on the outer membrane leaflet of NCC. NCC treated with this isolate had very high levels of cellular necrosis compared to all other isolates. This cellular pathology was confirmed by observing reduced DNA laddering in these same treated cells. Transmission EM also showed characteristic necrotic cellular changes in treated cells. To determine if the (in vitro) PCD/apoptosis protective effects of #173 correlated with any in vivo activity, tilapia were injected IV with #173 and #164 (an Israeli type I strain). Following injection, purified NCC were tested (in vitro) for cytotoxicity against HL-60 target cells. Four significant observations were made : (i) fish injected with #173 had 100-400% increased cytotoxicity compared to #164 (ii) in vivo activation occurred within 5 minutes of injection; (iii) activation occurred only within the peripheral blood compartment; and (iv) the isolate that protected NCC from apoptosis in vitro caused in vivo activation of cytotoxicity. The levels of in vivo cytotoxicity responses are associated with certain pathogens (pathogen associated molecular patterns/PAMP) and with the tissue of origin of NCC. NCC from different tissue (i.e. PBL, anterior kidney, spleen) exist in different states of differentiation. Random amplified polymorphic DNA (RAPD) analysis revealed the "adaptation" of the bacterium to the vaccinated environment, suggesting a "Darwinian-like" evolution of any bacterium. Due to the selective pressure which has occurred in the vaccinated environment, type II strains, able to evade the protective response elicited by the vaccine, have evolved from type I strains. The increased virulence through the appropriation of a novel antigenic composition conforms with pathogenic mechanisms described for other streptococci. Vaccine efficacy was improved: water-in-oil formulations were found effective in inducing protection that lasted for a period of (at least) 6 months. Protection was evaluated by functional tests - the protective effect, and immunological parameters - elicitation of T- and B-cells proliferation. Vaccinated fish were found to be resistant to the disease for (at least) six months; protection was accompanied by activation of the cellular and the humoral branches.
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Sionov, Edward, Nancy Keller und Shiri Barad-Kotler. Mechanisms governing the global regulation of mycotoxin production and pathogenicity by Penicillium expansum in postharvest fruits. United States Department of Agriculture, Januar 2017. http://dx.doi.org/10.32747/2017.7604292.bard.
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The original objectives of the study, as defined in the approved proposal, are: To characterize the relationship of CreA and LaeA in regulation of P T production To understand how PacC modulates P. expansumpathogenicity on apples To examine if other secondary metabolites are involved in virulence or P. expansumfitness To identify the signaling pathways leading to PAT synthesis Penicilliumexpansum, the causal agent of blue mould rot, is a critical health concern because of the production of the mycotoxinpatulin (PAT) in colonized apple fruit tissue. Although PAT is produced by many Penicilliumspecies, the factors activating its biosynthesis were not clear. This research focused on host and fungal mechanisms of activation of LaeA (the global regulator of secondary metabolism), PacC (the global pH modulator) and CreA (the global carbon catabolite regulator) on PAT synthesis with intention to establish P. expansumas the model system for understanding mycotoxin synthesis in fruits. The overall goal of this proposal is to identify critical host and pathogen factors that mechanistically modulate P. expansumgenes and pathways to control activation of PAT production and virulence in host. Several fungal factors have been correlated with disease development in apples, including the production of PAT, acidification of apple tissue by the fungus, sugar content and the global regulator of secondary metabolism and development, LaeA. An increase in sucrose molarity in the culture medium from 15 to 175 mM negatively regulated laeAexpression and PAT accumulation, but, conversely, increased creAexpression, leading to the hypothesis that CreA could be involved in P. expansumPAT biosynthesis and virulence, possibly through the negative regulation of LaeA. We found evidence for CreAtranscriptional regulation of laeA, but this was not correlated with PAT production either in vitro or in vivo, thus suggesting that CreA regulation of PAT is independent of LaeA. Our finding that sucrose, a key ingredient of apple fruit, regulates PAT synthesis, probably through suppression of laeAexpression, suggests a potential interaction between CreA and LaeA, which may offer control therapies for future study. We have also identified that in addition to PAT gene cluster, CreA regulates other secondary metabolite clusters, including citrinin, andrastin, roquefortine and communesins, during pathogenesis or during normal fungal growth. Following creation of P. expansumpacCknockout strain, we investigated the involvement of the global pH regulator PacC in fungal pathogenicity. We demonstrated that disruption of the pH signaling transcription factor PacC significantly decreased the virulence of P. expansumon deciduous fruits. This phenotype is associated with an impairment in fungal growth, decreased accumulation of gluconic acid and reduced synthesis of pectolytic enzymes. We showed that glucose oxidase- encoding gene, which is essential for gluconic acid production and acidification during fruit colonization, was significantly down regulated in the ΔPepacCmutant, suggesting that gox is PacC- responsive gene. We have provided evidence that deletion of goxgene in P. expansumled to a reduction in virulence toward apple fruits, further indicating that GOX is a virulence factor of P. expansum, and its expression is regulated by PacC. It is also clear from the present data that PacC in P. expansumis a key factor for the biosynthesis of secondary metabolites, such as PAT. On the basis of RNA-sequencing (RNA-seq) analysis and physiological experimentation, the P. expansumΔlaeA, ΔcreAand ΔpacCmutants were unable to successfully colonize apples for a multitude of potential mechanisms including, on the pathogen side, a decreased ability to produce proteolytic enzymes and to acidify the environment and impaired carbon/nitrogen metabolism and, on the host side, an increase in the oxidative defence pathways. Our study defines these global regulatory factors and their downstream signalling pathways as promising targets for the development of strategies to fight against this post-harvest pathogen.
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Shpigel, Nahum Y., Ynte Schukken und Ilan Rosenshine. Identification of genes involved in virulence of Escherichia coli mastitis by signature tagged mutagenesis. United States Department of Agriculture, Januar 2014. http://dx.doi.org/10.32747/2014.7699853.bard.
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Mastitis, an inflammatory response of the mammary tissue to invading pathogenic bacteria, is the largest health problem in the dairy industry and is responsible for multibillion dollar economic losses. E. coli are a leading cause of acute mastitis in dairy animals worldwide and certainly in Israel and North America. The species E. coli comprises a highly heterogeneous group of pathogens, some of which are commensal residents of the gut, infecting the mammary gland after contamination of the teat skin from the environment. As compared to other gut microflora, mammary pathogenic E. coli (MPEC) may have undergone evolutionary adaptations that improve their fitness for colonization of the unique and varied environmental niches found within the mammary gland. These niches include competing microbes already present or accompanying the new colonizer, soluble and cellular antimicrobials in milk, and the innate immune response elicited by mammary cells and recruited immune cells. However, to date, no specific virulence factors have been identified in E. coli isolates associated with mastitis. The original overall research objective of this application was to develop a genome-wide, transposon-tagged mutant collection of MPEC strain P4 and to use this technology to identify E. coli genes that are specifically involved in mammary virulence and pathogenicity. In the course of the project we decided to take an alternative genome-wide approach and to use whole genomes bioinformatics analysis. Using genome sequencing and analysis of six MPEC strains, our studies have shown that type VI secretion system (T6SS) gene clusters were present in all these strains. Furthermore, using unbiased screening of MPEC strains for reduced colonization, fitness and virulence in the murine mastitis model, we have identified in MPEC P4-NR a new pathogenicity island (PAI-1) encoding the core components of T6SS and its hallmark effectors Hcp, VgrG and Rhs. Next, we have shown that specific deletions of T6SS genes reduced colonization, fitness and virulence in lactating mouse mammary glands. Our long-term goal is to understand the molecular mechanisms of host-pathogen interactions in the mammary gland and to relate these mechanisms to disease processes and pathogenesis. We have been able to achieve our research objectives to identify E. coli genes that are specifically involved in mammary virulence and pathogenicity. The project elucidated a new basic concept in host pathogen interaction of MPEC, which for the best of our knowledge was never described or investigated before. This research will help us to shed new light on principles behind the infection strategy of MPEC. The new targets now enable prevalence and epidemiology studies of T6SS in field strains of MPEC which might unveil new geographic, management and ecological risk factors. These will contribute to development of new approaches to treat and prevent mastitis by MPEC and perhaps other mammary pathogens. The use of antibiotics in farm animals and specifically to treat mastitis is gradually precluded and thus new treatment and prevention strategies are needed. Effective mastitis vaccines are currently not available, structural components and effectors of T6SS might be new targets for the development of novel vaccines and therapeutics.
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Dickman, Martin B., und Oded Yarden. Modulation of the Redox Climate and Phosphatase Signaling in a Necrotroph: an Axis for Inter- and Intra-cellular Communication that Regulates Development and Pathogenicity. United States Department of Agriculture, August 2011. http://dx.doi.org/10.32747/2011.7697112.bard.
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The long-term goals of our research are to understand the regulation of sclerotial development and pathogenicity in S. sclerotiorum. The focus in this project is on the elucidation of the signaling events and environmental cues that contribute to broad pathogenic success of S. sclerotiorum. In this proposal, we have taken advantage of the recent conceptual (ROS/PPs signaling) and technical (genome sequence availability and gene inactivation possibilities) developments to address the following questions, as appear in our research goals stated below, specifically concerning the involvement of REDOX signaling and protein dephosphorylation in the regulation of hyphal/sclerotial development and pathogenicity of S. sclerotiorum. Our stated specific objectives were to progress our understanding of the following questions: (i) Which ROS species affect S. sclerotiorum development and pathogenicity? (ii) In what manner do PPs affect S. sclerotiorum development and pathogenicity? (iii) Are PPs affected by ROS production and does PP activity affect ROS production and SMK1? (iv) How does Sclerotinia modulate the redox environment in both host and pathogen? While addressing these questions, our main findings include the identification and characterization the NADPH oxidase (NOX) family in S. sclerotiorum. Silencing of Ssnox1 indicated a central role for this enzyme in both virulence and pathogenic (sclerotial) development, while inactivation of Ssnox2 resulted in limited sclerotial development but remained fully pathogenic. Interestingly, we found a consistent correlation with Ssnox1(involved with pathogenicity) and oxalate levels. This same observation was also noted with Sssod1. Thus, fungal enzymes involved in oxidative stress tolerance,when inactivated, also exhibit reduced OA levels. We have also shown that protein phosphatases (specifically PP2A and PTP1) are involved in morphogenesis and pathogenesis of S. sclerotiorum, demonstrating the regulatory role of these key proteins in the mentioned processes. While probing the redox environment and host-pathogen interactions we determined that oxalic acid is an elicitor of plant programmed cell death during S. sclerotiorum disease development and that oxalic acid suppresses host defense via manipulation of the host redox environment. During the course of this project we also contributed to the progress of understanding S. sclerotiorum function and the manipulation of this fungus by establishing an efficient gene replacement and direct hyphal transformation protocols in S. sclerotiorum. Lastly, both PIs were involved in thegenomic analysis of this necrotrophic fungal pathogen (along with Botrytis cinerea). Our results have been published in 11 papers (including joint papers and refereed reviews) and have set the basis for a continuum towards a better understanding and eventual control of this important pathogen (with implications to other fungal-host systems as well).
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Harms, Nathan, Judy Shearer, James Cronin und John Gaskin. Geographic and genetic variation in susceptibility of Butomus umbellatus to foliar fungal pathogens. Engineer Research and Development Center (U.S.), August 2021. http://dx.doi.org/10.21079/11681/41662.
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Large-scale patterns of plant invasions may reflect regional heterogeneity in biotic and abiotic factors and genetic variation within and between invading populations. Having information on how effects of biotic resistance vary spatially can be especially important when implementing biological control because introduced agents may have different Impacts through interactions with host-plant genotype, local environment, or other novel enemies. We conducted a series of field surveys and laboratory studies to determine whether there was evidence of biotic resistance, as foliar fungal pathogens, in two introduced genotypes (triploid G1, diploid G4) of the Eurasian wetland weed, Butomus umbellatus L. in the USA. We tested whether genotypes differed in disease attack and whether spatial patterns in disease incidence were related to geographic location or climate for either genotype. After accounting for location (latitude, climate), G1 plants had lower disease incidence than G4 plants in the field (38% vs. 70%) but similar pathogen richness. In contrast, bioassays revealed G1 plants consistently received a higher damage score and had larger leaf lesions regardless of pathogen. These results demonstrate that two widespread B. umbellatus genotypes exhibit different susceptibility to pathogens and effectiveness of pathogen biological controls may depend on local conditions.
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Prusky, Dov, und Jeffrey Rollins. Modulation of pathogenicity of postharvest pathogens by environmental pH. United States Department of Agriculture, Dezember 2006. http://dx.doi.org/10.32747/2006.7587237.bard.
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Until recently, environmental pH was not considered a factor in determining pathogen compatibility. Our hypothesis was that the environmental pH at the infection site, which is dynamically controlled by activities of both the host and the pathogen, regulates the expression of genes necessary for disease development in Colletotrichum gloeosporioides and Sclerotinia sclerotiorum. This form of regulation ensures that genes are expressed at optimal conditions for their encoded activities.Pectate lyase encoded by pelB, has been demonstrated to play a key role in virulence of C. gloeosporioides in avocado fruit. Polyglacturonase synergism with oxalic acid production is considered to be an essential pathogenicity determinant in the interactions of S. sclerotiorum with its numerous hosts. A common regulatory feature of these virulence and pathogenicity factors is their dependence upon environmental pH conditions within the host niche to create optimal conditions for expression and secretion. In this proposal we have examined, 1) the mechanisms employed by these fungi to establish a suitable pH environment, 2) the molecular levels at which genes and gene products are regulated in response to environmental pH, and 3) the molecular basis and functional importance of pH-responsive gene regulation during pathogenicity. The specific objectives of the proposal were: 1. Characterize the mechanism of local pH modulation and the effect of ambient pH on the expression and secretion of virulence factors. 2. Provide evidence that a conserved molecular pathway for pH-responsive gene expression exists in C. gloeosporioides by cloning a pacC gene homologue. 3. Determine the role of pacC in pathogenicity by gene disruption and activating mutations. Major conclusions 1. We determined the importance of nitrogen source and external pH in the secretion of the virulence factor pectate lyase with respect to the ambient pH transcriptional regulator pacC. It was concluded that nitrogen source availability and ambient pH are two independent signals for the transcriptional regulation of genes required for the disease process of C. gloeosporioides and possibly of other pathogens. 2. We also determined that availability of ammonia regulate independently the alkalinization process and pelB expression, pecate lyase secretion and virulence of C. gloeosporioides. 3. Gene disruption of pacC reduced virulence of C. gloeosporioides however did not reduced fully pelB expression. It was concluded that pelB expression is regulated by several factors including pH, nitrogen and carbon sources. 4. Gene disruption of pacC reduced virulence of S. slcerotiourum Creation of a dominant activating