Academic literature on the topic 'Pathogen adaptation'
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Journal articles on the topic "Pathogen adaptation":
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Fonville, Judith M. "Expected Effect of Deleterious Mutations on Within-Host Adaptation of Pathogens." Journal of Virology 89, no. 18 (June 24, 2015): 9242–51. http://dx.doi.org/10.1128/jvi.00832-15.
Abstract:
ABSTRACTAdaptation is a common theme in both pathogen emergence, for example, in zoonotic cross-species transmission, and pathogen control, where adaptation might limit the effect of the immune response and antiviral treatment. When such evolution requires deleterious intermediate mutations, fitness ridges and valleys arise in the pathogen's fitness landscape. The effect of deleterious intermediate mutations on within-host pathogen adaptation is examined with deterministic calculations, appropriate for pathogens replicating in large populations with high error rates. The effect of deleterious intermediate mutations on pathogen adaptation is smaller than their name might suggest: when two mutations are required and each individual single mutation is fully deleterious, the pathogen can jump across the fitness valley by obtaining two mutations at once, leading to a proportion of adapted mutants that is 20-fold lower than that in the situation where the fitness of all mutants is neutral. The negative effects of deleterious intermediates are typically substantially smaller and outweighed by the fitness advantages of the adapted mutant. Moreover, requiring a specific mutation order has a substantially smaller effect on pathogen adaptation than the effect of all intermediates being deleterious. These results can be rationalized when the number of routes of mutation available to the pathogen is calculated, providing a simple approach to estimate the effect of deleterious mutations. The calculations discussed here are applicable when the effect of deleterious mutations on the within-host adaptation of pathogens is assessed, for example, in the context of zoonotic emergence, antigenic escape, and drug resistance.IMPORTANCEAdaptation is critical for pathogens after zoonotic transmission into a new host species or to achieve antigenic immune escape and drug resistance. Using a deterministic approach, the effects of deleterious intermediate mutations on pathogen adaptation were calculated while avoiding commonly made simplifications that do not apply to large pathogen populations replicating with high mutation rates. Perhaps unexpectedly, pathogen adaptation does not halt when the intermediate mutations are fully deleterious. The negative effects of deleterious mutations are substantially outweighed by the fitness gains of adaptation. To gain an understanding of the effect of deleterious mutations on pathogen adaptation, a simple approach that counts the number of routes available to the pathogen with and without deleterious intermediate mutations is introduced. This methodology enables a straightforward calculation of the proportion of the pathogen population that will cross a fitness valley or traverse a fitness ridge, without reverting to more complicated mathematical models.
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Sánchez-Vallet, Andrea, Simone Fouché, Isabelle Fudal, Fanny E. Hartmann, Jessica L. Soyer, Aurélien Tellier, and Daniel Croll. "The Genome Biology of Effector Gene Evolution in Filamentous Plant Pathogens." Annual Review of Phytopathology 56, no. 1 (August 25, 2018): 21–40. http://dx.doi.org/10.1146/annurev-phyto-080516-035303.
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Filamentous pathogens, including fungi and oomycetes, pose major threats to global food security. Crop pathogens cause damage by secreting effectors that manipulate the host to the pathogen's advantage. Genes encoding such effectors are among the most rapidly evolving genes in pathogen genomes. Here, we review how the major characteristics of the emergence, function, and regulation of effector genes are tightly linked to the genomic compartments where these genes are located in pathogen genomes. The presence of repetitive elements in these compartments is associated with elevated rates of point mutations and sequence rearrangements with a major impact on effector diversification. The expression of many effectors converges on an epigenetic control mediated by the presence of repetitive elements. Population genomics analyses showed that rapidly evolving pathogens show high rates of turnover at effector loci and display a mosaic in effector presence-absence polymorphism among strains. We conclude that effective pathogen containment strategies require a thorough understanding of the effector genome biology and the pathogen's potential for rapid adaptation.
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VanHook, Annalisa M. "Pathogen rewiring for host adaptation." Science 370, no. 6517 (November 5, 2020): 677.20–679. http://dx.doi.org/10.1126/science.370.6517.677-t.
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Slev, Patricia R., and Wayne K. Potts. "Disease consequences of pathogen adaptation." Current Opinion in Immunology 14, no. 5 (October 2002): 609–14. http://dx.doi.org/10.1016/s0952-7915(02)00381-3.
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Laine, Anna-Liisa, Jeremy J. Burdon, Adnane Nemri, and Peter H. Thrall. "Host ecotype generates evolutionary and epidemiological divergence across a pathogen metapopulation." Proceedings of the Royal Society B: Biological Sciences 281, no. 1787 (July 22, 2014): 20140522. http://dx.doi.org/10.1098/rspb.2014.0522.
Abstract:
The extent and speed at which pathogens adapt to host resistance varies considerably. This presents a challenge for predicting when—and where—pathogen evolution may occur. While gene flow and spatially heterogeneous environments are recognized to be critical for the evolutionary potential of pathogen populations, we lack an understanding of how the two jointly shape coevolutionary trajectories between hosts and pathogens. The rust pathogen Melampsora lini infects two ecotypes of its host plant Linum marginale that occur in close proximity yet in distinct populations and habitats. In this study, we found that within-population epidemics were different between the two habitats. We then tested for pathogen local adaptation at host population and ecotype level in a reciprocal inoculation study. Even after controlling for the effect of spatial structure on infection outcome, we found strong evidence of pathogen adaptation at the host ecotype level. Moreover, sequence analysis of two pathogen infectivity loci revealed strong genetic differentiation by host ecotype but not by distance. Hence, environmental variation can be a key determinant of pathogen population genetic structure and coevolutionary dynamics and can generate strong asymmetry in infection risks through space.
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Hanford, Hannah E., Juanita Von Dwingelo, and Yousef Abu Kwaik. "Bacterial nucleomodulins: A coevolutionary adaptation to the eukaryotic command center." PLOS Pathogens 17, no. 1 (January 21, 2021): e1009184. http://dx.doi.org/10.1371/journal.ppat.1009184.
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Through long-term interactions with their hosts, bacterial pathogens have evolved unique arsenals of effector proteins that interact with specific host targets and reprogram the host cell into a permissive niche for pathogen proliferation. The targeting of effector proteins into the host cell nucleus for modulation of nuclear processes is an emerging theme among bacterial pathogens. These unique pathogen effector proteins have been termed in recent years as “nucleomodulins.” The first nucleomodulins were discovered in the phytopathogensAgrobacteriumandXanthomonas, where their nucleomodulins functioned as eukaryotic transcription factors or integrated themselves into host cell DNA to promote tumor induction, respectively. Numerous nucleomodulins were recently identified in mammalian pathogens. Bacterial nucleomodulins are an emerging family of pathogen effector proteins that evolved to target specific components of the host cell command center through various mechanisms. These mechanisms include: chromatin dynamics, histone modification, DNA methylation, RNA splicing, DNA replication, cell cycle, and cell signaling pathways. Nucleomodulins may induce short- or long-term epigenetic modifications of the host cell. In this extensive review, we discuss the current knowledge of nucleomodulins from plant and mammalian pathogens. While many nucleomodulins are already identified, continued research is instrumental in understanding their mechanisms of action and the role they play during the progression of pathogenesis. The continued study of nucleomodulins will enhance our knowledge of their effects on nuclear chromatin dynamics, protein homeostasis, transcriptional landscapes, and the overall host cell epigenome.
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Fedderke, Johannes W., Robert E. Klitgaard, and Valerio Napolioni. "Genetic adaptation to historical pathogen burdens." Infection, Genetics and Evolution 54 (October 2017): 299–307. http://dx.doi.org/10.1016/j.meegid.2017.07.017.
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TASARA, T., and R. STEPHAN. "Cold Stress Tolerance of Listeria monocytogenes: A Review of Molecular Adaptive Mechanisms and Food Safety Implications." Journal of Food Protection 69, no. 6 (June 1, 2006): 1473–84. http://dx.doi.org/10.4315/0362-028x-69.6.1473.
Abstract:
The foodborne pathogen Listeria monocytogenes has many physiological adaptations that enable survival under a wide range of environmental conditions. The microbes overcome various types of stress, including the cold stress associated with low temperatures in food-production and storage environments. Cold stress adaptation mechanisms are therefore an important attribute of L. monocytogenes, enabling these food pathogens to survive and proliferate to reach minimal infectious levels on refrigerated foods. This phenomenon is a function of many molecular adaptation mechanisms. Therefore, an improved understanding of how cold stress is sensed and adaptation measures implemented by L. monocytogenes may facilitate the development of better ways of controlling these pathogens in food and related environments. Research over the past few years has highlighted some of the molecular aspects of cellular mechanisms behind cold stress adaptation in L. monocytogenes. This review provides an overview of the molecular and physiological constraints of cold stress and discusses the various cellular cold stress response mechanisms in L. monocytogenes, as well as their implications for food safety.
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Henschen, Amberleigh E., Michal Vinkler, Marissa M. Langager, Allison A. Rowley, Rami A. Dalloul, Dana M. Hawley, and James S. Adelman. "Rapid adaptation to a novel pathogen through disease tolerance in a wild songbird." PLOS Pathogens 19, no. 6 (June 9, 2023): e1011408. http://dx.doi.org/10.1371/journal.ppat.1011408.
Abstract:
Animal hosts can adapt to emerging infectious disease through both disease resistance, which decreases pathogen numbers, and disease tolerance, which limits damage during infection without limiting pathogen replication. Both resistance and tolerance mechanisms can drive pathogen transmission dynamics. However, it is not well understood how quickly host tolerance evolves in response to novel pathogens or what physiological mechanisms underlie this defense. Using natural populations of house finches (Haemorhous mexicanus) across the temporal invasion gradient of a recently emerged bacterial pathogen (Mycoplasma gallisepticum), we find rapid evolution of tolerance (<25 years). In particular, populations with a longer history of MG endemism have less pathology but similar pathogen loads compared with populations with a shorter history of MG endemism. Further, gene expression data reveal that more-targeted immune responses early in infection are associated with tolerance. These results suggest an important role for tolerance in host adaptation to emerging infectious diseases, a phenomenon with broad implications for pathogen spread and evolution.
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Hoque, M. Mozammel, Parisa Noorian, Gustavo Espinoza-Vergara, Pradeep Manuneedhi Cholan, Mikael Kim, Md Hafizur Rahman, Maurizio Labbate, et al. "Adaptation to an amoeba host drives selection of virulence-associated traits in Vibrio cholerae." ISME Journal 16, no. 3 (October 15, 2021): 856–67. http://dx.doi.org/10.1038/s41396-021-01134-2.
Abstract:
AbstractPredation by heterotrophic protists drives the emergence of adaptive traits in bacteria, and often these traits lead to altered interactions with hosts and persistence in the environment. Here we studied adaptation of the cholera pathogen, Vibrio cholerae during long-term co-incubation with the protist host, Acanthamoeba castellanii. We determined phenotypic and genotypic changes associated with long-term intra-amoebal host adaptation and how this impacts pathogen survival and fitness. We showed that adaptation to the amoeba host leads to temporal changes in multiple phenotypic traits in V. cholerae that facilitate increased survival and competitive fitness in amoeba. Genome sequencing and mutational analysis revealed that these altered lifestyles were linked to non-synonymous mutations in conserved regions of the flagellar transcriptional regulator, flrA. Additionally, the mutations resulted in enhanced colonisation in zebrafish, establishing a link between adaptation of V. cholerae to amoeba predation and enhanced environmental persistence. Our results show that pressure imposed by amoeba on V. cholerae selects for flrA mutations that serves as a key driver for adaptation. Importantly, this study provides evidence that adaptive traits that evolve in pathogens in response to environmental predatory pressure impact the colonisation of eukaryotic organisms by these pathogens.
Dissertations / Theses on the topic "Pathogen adaptation":
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Bacigalupe, Rodrigo. "Population genomic analysis of bacterial pathogen niche adaptation." Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31266.
Abstract:
Globally disseminated bacterial pathogens frequently cause epidemics that are of major importance in public health. Of particular significance is the capacity for some of these bacteria to switch into a new environment leading to the emergence of pathogenic clones. Understanding the evolution and epidemiology of such pathogens is essential for designing rational ways for prevention, diagnosis and treatment of the diseases they cause. Whole-genome sequencing of multiple isolates facilitating comparative genomics and phylogenomic analyses provides high-resolution insights, which are revolutionizing our understanding of infectious diseases. In this thesis, a range of population genomic analyses are employed to study the molecular mechanisms and the evolutionary dynamics of bacterial pathogen niche adaptation, specifically between humans, animals and the environment. A large-scale population genomic approach was used to provide a global perspective of the host-switching events that have defined the evolution of Staphylococcus aureus in the context of its host-species. To investigate the genetic basis of host-adaptation, we performed genome-wide association analysis, revealing an array of accessory genes linked to S. aureus host-specificity. In addition, positive selection analysis identified biological pathways encoded in the core genome that are under diversifying selection in different host-species, suggesting a role in host-adaptation. These findings provide a high-resolution view of the evolutionary landscape of a model multi-host pathogen and its capacity to undergo changes in host ecology by genetic adaptation. To further explore S. aureus host-adaptive evolution, we examined the population dynamics of this pathogen after a simulated host-switch event. S. aureus strains of human origin were used to infect the mammary glands of sheep, and bacteria were passaged in multiple animals to simulate onward transmission events. Comparative genomics of passaged isolates allowed us to characterize the genetic changes acquired during the early stages of evolution in a novel host-species. Co-infection experiments using progenitor and passaged strains indicated that accumulated mutations contributed to enhanced fitness, indicating adaptation. Within-host population genomic analysis revealed the existence of population bottlenecks associated with transmission and establishment of infection in new hosts. Computational simulations of evolving genomes under regular bottlenecks supported that the fitness gain of beneficial mutations is high enough to overcome genetic drift and sweep through the population. Overall, these data provide new information relating to the critical early events associated with adaptation to novel host-species. Finally, population genomics was used to study the total diversity of Legionella longbeachae from patient and environmental sources and to investigate the epidemiology of a L. longbeachae outbreak in Scotland. We analysed the genomes of isolates from a cluster of legionellosis cases linked to commercial growing media in Scotland and of non-outbreak-associated strains from this and other countries. Extensive genetic diversity across the L. longbeachae species was identified, associated with intraspecies and interspecies gene flow, and a wide geographic distribution of closely related genotypes. Of note, a highly diverse pool of L. longbeachae genotypes within compost samples that precluded the genetic establishment of an infection source was observed. These data represent a view of the genomic diversity of this pathogen that will inform strategies for investigating future outbreaks. Overall, our findings demonstrate the application of population genomics to understand the molecular mechanisms and the evolutionary dynamics of bacterial adaptation to different ecological niches, and provide new insights relevant to other major bacterial pathogens with the capacity to spread between environments.
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Amezaga, Herran Maria Rosario. "The adaptation of Listeria monocytogenes to osmotic stress." Thesis, University of Aberdeen, 1996. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU602297.
Abstract:
The food-borne pathogen Listeria monocytogenes is more salt tolerant in the complex medium brain heart infusion (BHI, 2.0M NaCI upper limit for growth) than in a chemically-defined medium (DM, 1.0M NaCI upper limit for growth). The components in BHI responsible for the characteristic salt tolerance of L. monocytogenes are peptone and glycine betaine. At high osmolarity, the growth stimulation by peptone was higher than expected from nutritional supplementation, indicating that an osmoprotective mechanism was also at play. Peptone provided a higher level of osmotic protection than the compatible solute glycine betaine which was a moderate osmoprotectant. Our growth data demonstrated that of the free amino acids and peptides contained in peptone it is the peptides which are the osmoprotectants for L monocytogenes. Furthermore, specific peptides, such as PGG (prolyl-glycyl- glycine) and PHP (prolyl-hydroxyproline), behaved in growth experiments as the compatible solute glycine betaine, i.e. stimulation of growth at high osmolarity and no effect at low osmolarity. Our analysis of the changes in the intracellular pools of amino acids, under conditions of sosmotic stress, when peptone or specific peptide are supplied to the growth medium, has shown the following features in the mechanism of adaptation of L. monocytogenes to osmotic stress: i) Peptides are taken up, by at least two specific transport systems. ii) Subsequently, peptides are hydrolysed intracellularly by peptidases. iii) As a consequence of ii), a significant increase in the pool of free amino acids occurs. Osmoadaptation in L. monocytogenes iv) We have also demonstrated that depending on the nature of the constituent amino acids, some peptides are not fully hydrolysed which leads to the accumulation of an intracellular peptide pool in L. monocytogenes. v) Proline, glycine and hydroxyproline are the amino acids preferentially accumulated as free amino acids or as part of peptides. vi) The intracellular accumulation of free amino acids and peptides is positively correlated to an increase in the external osmolarity and has an important role in the osmoadaptation of L. monocytogenes.
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Boixel, Anne-Lise. "Environmental heterogeneity, a driver of adaptation to temperature in foliar plant pathogen populations?" Thesis, université Paris-Saclay, 2020. http://www.theses.fr/2020UPASA010.
Abstract:
Les facteurs environnementaux, au premier rang desquels la température, ont un impact sur la biologie des micro-organismes foliaires. Ils peuvent aussi modifier significativement leurs dynamiques populationnelles, voire leurs trajectoires évolutives. Classiquement, les modèles épidémiologiques, utilisés pour mieux gérer les maladies des plantes, intègrent l’influence des conditions météorologiques. Ils s’intéressent surtout à des réponses et des effets moyennés, ne tenant compte ni des variations des réponses individuelles, ni de l’hétérogénéité des changements environnementaux aux échelles réellement perçues par les agents pathogènes. Ces deux niveaux de simplification sont acceptables lorsque les états individuels et les variables continues qui leur sont associées, peu diversifiés, sont représentatifs de ceux de l'ensemble de la population. Il en va différemment lorsque les populations présentent des niveaux substantiels de variation individuelle susceptibles d’influencer leur capacité à s’adapter à leur environnement, et, par voie de conséquence, la dynamique des épidémies sous un climat fluctuant ou changeant. Pour mettre en évidence les conséquences de ces hypothèses réductrices, j’ai étudié comment la variation individuelle et l'hétérogénéité environnementale affectent simultanément la fitness, la composition phénotypique et la résilience des populations d'un agent pathogène foliaire (Zymoseptoria tritici) dans des couverts de blé. Trois étapes clés ont structuré l’exploration de ce cas d’étude. Tout d’abord, un protocole in vitro de phénotypage haut débit a été spécifiquement développé, validé et utilisé pour caractériser la diversité des réponses à la température de populations de Z. tritici échantillonnées à des échelles climatiques contrastées (variation spatiale et saisonnière) ainsi que leurs patrons d’adaptation. Les variations environnementales spatio-temporelles rencontrées dans les couverts de blé, considérées comme exerçant des pressions sélectives différentielles sur ces sensibilités thermiques individuelles, ont ensuite été examinées. Enfin, la façon dont la sélection de « thermotypes » (groupes fonctionnels rassemblant des individus présentant une même sensibilité thermique) détermine la dynamique adaptative des populations en réponse à l'hétérogénéité environnementale a été étudiée. Pour cela, des approches expérimentales (in vitro, in planta et in natura) et de modélisation (in silico) ont été couplées. Elles ont notamment porté sur plusieurs générations de populations placées dans des environnements sélectifs de plus en plus complexes. Ces travaux ont montré que le fait de négliger l'amplitude réelle de la variation phénotypique inter-individuelle d'une population microbienne et l'hétérogénéité des pressions de sélection, s’exerçant des échelles phyllo- à mésoclimatiques, conduit à sous-estimer la résilience de cette population, et donc son potentiel adaptatif. Les résultats de cette thèse, à l’interface entre épidémiologie, micrométéorologie et écologie, améliorent notre compréhension d’une part, de l'importance de la variation individuelle dans la dynamique adaptative des populations et, d’autre part, de la manière dont l'hétérogénéité environnementale permet de maintenir des populations globalement très diverses. Elle permet finalement d’expliquer l’existence de patrons d’adaptation, à la fois à des échelles locales et à des échelles très larges, par des dynamiques adaptatives «à deux vitesses»Environmental drivers, most notably temperature, affect the biology of phyllosphere microorganisms but also induce changes in their population dynamics, even in their evolutionary trajectories. The impact of climate on foliar plant disease epidemics is usually considered in forecasting models to inform management strategies. Such models focus on averages of environmental drivers but disregard both individual variation within populations and the scale and extent of biologically relevant environmental changes. These simplifications are glossing over substantial levels of individual variation that may have important consequences on the capacity of a population to adapt to environmental changes, and thus on the dynamics of epidemics in a fluctuating or changing climate. To examine the range of validity and consequences of these simplifying assumptions, I investigated how individual variation and environmental heterogeneity jointly affect fitness, phenotypic composition and resilience of populations of a foliar pathogen (Zymoseptoria tritici) inhabiting wheat canopies. Three complementary ways of exploration were adopted in this case study. First, an in vitro high-throughput phenotyping framework was developed, validated, and used to characterise the diversity in patterns of thermal responses existing across Z. tritici populations that were sampled over contrasted scales (spatial and seasonal variation of temperature). Second, the spatio-temporal thermal variations encountered in a wheat canopy, considered as a habitat exerting fluctuating selective pressures on these differential thermal sensitivities of individuals, were investigated in depth. Third, the way selection of “thermotypes” (functional groups of individuals displaying a similar thermal sensitivity) occurs and drives dynamics of Z. tritici populations was examined. To this end, both empirical (in vitro, in planta and in natura) and theoretical (in silico) competition experiments were conducted under increasingly complex selective environments. This research work demonstrates that glossing over the natural extent of individual phenotypic diversity in a phyllosphere microbial population and over the heterogeneity of selective pressures – from phyllo- to mesoclimate – leads to underestimate the resilience of this population, and thus its adaptive potential to environmental variations. In doing so, the results of this thesis, at the interface between epidemiology, micrometeorology, and ecology, improve our understanding of how important is individual variation to population dynamics and how environmental heterogeneity allows to maintain population diversity. Finally, this thesis provides insight into how large-scale patterns and local population processes are interlinked and display a “two-tier” adaptive dynamics
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Guillemet, Martin. "The dynamics of viral adaptation : theoretical and experimental approaches." Electronic Thesis or Diss., Université de Montpellier (2022-....), 2023. http://www.theses.fr/2023UMONG020.
Abstract:
La plupart des organismes vivants peuvent être infectés par des virus. Cette omniprésence est due à différents facteurs, notamment des taux de mutation élevés, des populations de grande taille et des temps de génération courts, qui permettent une adaptation rapide à des espèces hôtes très différentes. La dynamique de l'adaptation des populations virales résulte de l'interaction entre de multiples forces évolutives. Au cours de cette thèse, nous avons développé une combinaison d'approches théoriques et expérimentales pour démêler l'influence de certains de ces facteurs sur l'adaptation virale.Tout d'abord, nous avons exploré la dynamique de l'adaptation virale face à une population hôte homogène. Nous avons utilisé le modèle géométrique de Fisher et étudié les dynamiques évolutive et épidémiologique d'une population virale en modèle intra-hôte. Ce modèle permet d'explorer l'hypothèse de la mutagenèse létale: est-il possible de traiter les infections virales avec des médicaments mutagènes pour augmenter la charge de mutation au-delà d'un seuil qui peut entraîner l'extinction de la population? Nous montrons quels paramètres affectent le taux de mutation critique conduisant à l'extinction virale et nous montrons comment l'épidémiologie et l'évolution peuvent affecter la dynamique transitoire de la population virale à l'intérieur de l'hôte lorsqu'un seul trait du cycle de vie du virus (taux de transmission) est soumis à la sélection. Nous étendons ce cadre de modélisation à l'étude de l'évolution conjointe de la transmission et de la virulence au cours de l'adaptation d'un pathogène émergent.Deuxièmement, nous avons étudié l'adaptation virale dans des populations d'hôtes hétérogènes lorsque le virus se propage parmi une population diversifiée d'hôtes résistants. Nous avons étudié l'émergence évolutive des virus : les virus peuvent-ils éviter l'extinction par l'acquisition de mutations d'échappement leur permettant d'infecter certains des hôtes résistants de la population? Nous avons développé un modèle de naissance/mort pour prédire la probabilité d'émergence évolutive en fonction de la composition de la population d'hôtes. En particulier, nous montrons comment la proportion d'hôtes multi-résistants peut réduire le risque d'émergence évolutive de l'agent pathogène. Nous mettons certaines de ces prédictions à l'épreuve en utilisant des bactériophages se propageant dans des populations bactériennes. Nous manipulons la diversité de l'immunité CRISPR dans les bactéries Streptococcus thermophilus et nous confirmons l'influence clé de la résistance multiple sur le risque d'adaptation virale.Troisièmement, nous avons également étudié l'adaptation virale dans des environnements variables dans le temps où la population hôte est autorisée à coévoluer avec le virus. Dans ce projet expérimental, nous avons suivi l'adaptation des bactériophages au fur et à mesure qu'ils évoluaient avec l'immunité CRISPR des bactéries S. thermophilus. Nous suivons les changements adaptatifs réciproques dans lesquels les bactéries acquièrent de nouvelles couches de résistance (nouveaux spacers dans le locus CRISPR) et les phages acquièrent de nouvelles mutations d'échappement dans les protospacers correspondants. Cette expérience nous permet de suivre la dynamique de l'adaptation virale dans le temps et l'espace. Nous avons noté des asymétries significatives dans les capacités de compétition entre les différentes souches bactériennes. Cette compétition asymétrique a des conséquences dramatiques sur le maintien de la diversité de la résistance de l'hôte et sur la dynamique coévolutive avec le virus. Cette thèse démontre la possibilité d'utiliser l'évolution expérimentale en microcosmes microbiens pour explorer la validité de certaines prédictions théoriques sur la dynamique de l'adaptation virale. Cette validation expérimentale est particulièrement importante si l'on veut utiliser des modèles évolutifs pour faire des recommandations de santé publiqueMost living organisms on the tree of life can be infected by viruses. The ubiquity of viruses is driven by different factors including high mutation rates, high population sizes and low generation times, which allow for quick adaptation to very different host species. The dynamics of adaptation - the rate of change of the mean fitness of the viral population - results from the interplay between multiple evolutionary forces that may promote or hamper viral adaptation. But the interactions between these different factors may often be difficult to understand. During this PhD we developed a combination of theoretical and experimental approaches to disentangle the influence of some of these factors on viral adaptation.First, we explored the dynamics of viral adaptation to a homogeneous host population. We used Fisher’s Geometric Model of adaptation and studied the joint evolutionary and epidemiological dynamics of a viral population spreading in a host population. This modeled allowed us to explore the lethal mutagenesis hypothesis: is it possible to treat viral infections with mutagenic drugs to increase the mutation load of the viral population beyond a threshold that may result in the extinction of the within-host population? We show which parameters affect the critical mutation rate leading to viral extinction and we show how epidemiology and evolution can affect the transient within-host dynamics of the viral population when a single virus life-history trait (transmission rate) is under selection. We extend this modeling framework to study the joint evolution of transmission and virulence during the adaptation of an emerging pathogen. At the beginning of an epidemic, these two traits are expected to evolve independently but a trade-off may build up with viral adaptation.Second, we studied viral adaptation in heterogeneous host populations when the virus spreads among a diversified population of resistance host. We studied the evolutionary emergence of viruses: can viruses avoid extinction by the acquisition of escape mutations allowing them to infect some of the resistant hosts in the population? We developed a simple birth-death process to predict the probability of evolutionary emergence as a function of the composition of the host population. In particular, we show how the proportion of multiple resistant hosts can reduce the risk of pathogen evolutionary emergence. We put some of these predictions to the test using bacteriophages spreading in bacterial populations. We manipulate the diversity of CRISPR immunity in Streptococcus thermophilus bacteria and we confirm the key influence of multiple resistance on the risk of viral adaptation.Third, we also studied viral adaptation in time-varying environments where the host population is allowed to coevolve with the virus. In this experimental project we monitored the adaptation of bacteriophages as they coevolved with the CRISPR immunity of S. thermophilus bacteria. We track reciprocal adaptive changes in which bacteria acquire new layers of resistance (new spacers in the CRISPR array) and phages acquire new escape mutations in the corresponding protospacers. This experiment allows us to monitor the dynamics of viral adaptation across time and space. Interestingly, we find a significant asymmetries in competitive abilities among different bacterial strain in the absence of phage predation. This asymmetric competition has dramatic consequences on the maintenance of diversity of host resistance and on the coevolutionary dynamics with the virus. This thesis demonstrates the possibility to use experimental evolution with microbial microcosms to explore the validity of some theoretical predictions on the dynamics of viral adaptation. This experimental validation is particularly important if one wants to use evolutionary models to make public-health recommendations
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Kastora, Stavroula. "Novel regulators that control the adaptation of a major fungal pathogen to combinations of host signals." Thesis, University of Aberdeen, 2015. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=228983.
Abstract:
One of the major aims of this thesis was to identify novel regulators that drive C. albicans adaptation during growth under different nutrient and temperature conditions. The classical stress response cascades have been previously characterised under standardized, but physiologically irrelevant growth conditions (YPD at 30°C). In this study these pathways and other regulators were examined under more physiologically relevant inputs because metabolic plasticity and thermo-tolerance have been shown to affect stress adaptation (Arguelles et al., 1999; Brown et al., 2014; Cowen, 2009; Diezmann et al., 2014). In this study, we characterized 18.5% of the functional C. albicans ORFeome under 144 different stress conditions by employing a standardized system of robotic screening (Chapter 3). These screens highlighted extensive carbon and temperature-conditional regulators in C. albicans. We identified carbon-conditional contributions of the transcriptional regulators Sfp1 and Rtg3 to stress adaptation in this pathogenic fungus (Chapter 4). Sfp1 was found to regulate the expression of key stress regulators during growth on glucose, whereas Rtg3 induced the expression of these stress genes during growth on lactate. Our screens also revealed a distinct set of transcription factors, Hap43, Swi4, Sfp1, Cap1 and Zcf31, that control regulators of cell wall integrity and that promote antifungal drug resistance in a temperature dependent and yet Hsp90- independent manner. The screens also provided new information about a relatively obscure group of transcriptional regulators in C. albicans; the zinc cluster proteins with focus on Zcf3 and Zcf18 which we further pursued with RNA-sequencing to establish them as modulators of cell cycle, stress resistance and virulence in C. albicans. Lastly, our screens reveal a network of regulators that are homologous to human oncogenes and control fungal growth via modulation of TOR signaling. In conclusion, this thesis has revealed many novel targets for possible antifungal drug development and highlighted the extensive and intricate cross-talk between stress response modules facilitated by physiologically relevant nutrient sources and ambient temperatures.
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Melnyk, Anita. "The Evolution of Antibiotic Resistance in Experimental Populations of Bacteria." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34556.
Abstract:
Antibiotic resistance is a major threat to public health. Understanding how it evolves,
and the genes that underlie resistance, is the main goal of my Ph.D. research. After a resistance mutation arises, it’s fate within a pathogen population will be etermined in part by its fitness: mutations that suffer little or no fitness cost are more likely to persist in the absence of antibiotic treatment. My research centers on understanding this process better by gaining knowledge about the spectrum of fitness effects associated with antibiotic resistance mutations.
Using a meta-analysis framework I find that, across a range of antibiotics and pathogens, on average single resistance mutations exhibit fitness costs in the absence of drug, however, there are instances of cost-free mutations. To evaluate the conditions leading to the persistence of resistance in the absence of antibiotic, I use experimental evolution of the opportunistic pathogen Pseudomonas aeruginosa and the antibiotic ciprofloxacin to investigate the phenotypic and genetic differences associated with constant and fluctuating drug treatment. I find that fluctuating drug treatment leads to the evolution of cost-free resistance. At the genetic level, cost-free resistance is the result of second-site mutations that compensate for the fitness cost associated with ciprofloxacin-resistance mutations. Further examination of the resistance mutations shows a lack of epistatic interactions between co-occurring mutations that confer resistance within a single isolate. To investigate the repeatability of the genetic causes of resistance, I execute a second evolution experiment using multiple clinical strains of P. aeruginosa adapting to a constant ciprofloxacin selective pressure. I find a remarkable lack of parallel evolution at the genomic level both within and between different P. aeruginosa strains.
I have shown that antibiotic resistance is costly, and that these costs can be ameliorated by second-site mutations that readily arise over short time scales. Additionally, different strains of the same bacteria can gain resistance through a diverse set of genetic mutations. On an applied level these results are not positive; combating resistance evolution will be difficult because pathogens can easily compensate fitness costs of resistance, and resistance itself can be gained via a large number of genetic targets.
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McDougald, S. Diane School of Microbiology & Immunology UNSW. "Regulation of starvation and nonculturability in the marine pathogen, Vibrio vulnificus." Awarded by:University of New South Wales. School of Microbiology and Immunology, 2000. http://handle.unsw.edu.au/1959.4/19118.
Abstract:
Vibrio vulnificus is a model environmental organism exhibiting a classical starvation response during nutrient limitation as well as a non-culturable state when exposed to low temperatures. In addition to these classic global responses, this organism is an opportunistic pathogen that exhibits numerous virulence factors. This organism was chosen as the model organism for the identification of regulators of the viable but nonculturable response (VBNC) and the starvation-induced maintenance of culturability (SIMC) that occurs when cells are starved prior to low temperature incubation. In order to accomplish this, three indirect approaches were used; proteomics, investigation of intercellular signalling pathways and genetic analysis of regulators involved in these responses. Two-dimensional gel electrophoresis was used to identify proteins expressed under conditions that induced SIMC. It was determined that carbon and long-term phosphorus starvation were important in the SIMC response. V. vulnificus was shown to possess genes, luxS and smcR, that are homologues of genes involved in signalling system system 2 in Vibrio harveyi. Signal molecules were produced upon starvation and the entry to stationary phase in V. vulnificus. Furthermore, a null mutation in smcR, a transcriptional regulator was shown to have pleiotropic effects in V. vulnificus, including up-regulation of numerous virulence factors and a defect in starvation survival and development of the SIMC response. We propose that V. vulnificus possesses a signalling system analogous to that of system 2 in V. harveyi, and that this system is involved in the regulation of stationary phase and starvation adaptation in this organism.
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Maikova, Anna. "The CRISPR-Cas system of human pathogen Clostridium difficile : function and regulation." Thesis, Université de Paris (2019-....), 2019. http://www.theses.fr/2019UNIP7091.
Abstract:
Clostridium difficile (nouveau nom Clostridioides difficile) est une bactérie à Gram-positif, sporulante, anaérobie stricte, présente dans le sol et les environnements aquatiques, ainsi que dans le tractus intestinal des mammifères. C. difficile est l’un des principaux clostridies pathogènes. Cette bactérie est devenue un vrai problème de santé publique associé à l'antibiothérapie dans les pays industrialisés. La diarrhée associée à C. difficile est actuellement la diarrhée nosocomiale la plus fréquente en Europe et dans le monde. Depuis la dernière décennie, la proportion de formes d’infections graves a augmentée en raison de l’émergence des souches hypervirulantes et épidémiques comme la souche R20291 de ribotype 027. L’infection à C. difficile provoque la diarrhée, la colite et même la mort. De nombreux aspects de la pathogenèse de C. difficile restent mal compris. En particulier, les mécanismes moléculaires de son adaptation aux conditions changeantes de l'hôte doivent être examinés.Durant le cycle d'infection, C. difficile survit dans des communautés intestinales riches en bactériophages, en utilisant des systèmes qui contrôlent les échanges génétiques favorisés dans ces environnements complexes. Au cours de la dernière décennie, les systèmes CRISPR (clustered regularly interspaced short palindromic repeats)-Cas (associés aux CRISPR) d'immunité adaptative chez les procaryotes contre des éléments génétiques exogènes sont devenus le centre d'intérêt scientifique parmi les divers systèmes de défense bactérienne.Des études antérieures ont révélé la présence d'ARN CRISPR abondants chez C. difficile. Cette bactérie possède un système CRISPR original, caractérisé par la présence d'un grand nombre de cassettes CRISPR (12 dans la souche 630 et 9 dans la souche hypervirulante R20291), de deux ou trois opérons cas conservés dans la majorité des génomes séquencés de C. difficile et la localisation au sein des prophages de plusieurs cassettes CRISPR. Cependant, le rôle de CRISPR-Cas dans la physiologie et le cycle infectieux de cet important pathogène reste obscur.Les objectifs de ce travail sont les suivants:1) étudier le rôle et la fonctionnalité du système CRISPR-Cas de C. difficile dans les interactions avec des éléments d'ADN étrangers (tels que les plasmides), 2) révéler la manière dont le système CRISPR-Cas de C. difficile est régulé et fonctionne dans des conditions de culture bactérienne différentes, incluant la réponse aux stress.Dans la présente thèse, la fonctionnalité du système CRISPR-Cas de C. difficile a été étudiée (chapitre 2). Grâce à des tests d'efficacité de conjugaison, la fonction défensive (en interférence) du système CRISPR-Cas a été démontrée. La corrélation entre les niveaux d'expression des ARN CRISPR et les niveaux d'interférence observés a également été montrée. De plus, grâce à la série d’expériences d’interférence, la fonctionnalité des motifs PAM (protospacer adjacent motifs) a été confirmée en accord avec des prédictions in silico. Le consensus fonctionnel de PAM a été déterminé expérimentalement avec les bibliothèques des plasmides. La fonction adaptative du système CRISPR-Cas de C. difficile a été également démontrée pour la souche de laboratoire. Le rôle de plusieurs opérons cas dans la fonctionnalité du système CRISPR de C. difficile est démontré aussi dans ce chapitre.Le chapitre 3 montre le lien entre le système CRISPR-Cas et un nouveau système toxine-antitoxine de type I, ainsi que leur possible co-régulation dans des conditions de biofilm et de stress. Ce chapitre définit également le rôle possible du c-di-GMP dans la régulation du système CRISPR-Cas de C. difficile. De plus, le chapitre 4 décrit l'utilisation du système CRISPR-Cas endogène comme nouvel outil pour la rédaction du génome de C. difficile.En conclusion, les données obtenues mettent en évidence les caractéristiques originales du système CRISPR-Cas actif de C. difficile et démontrent son potentiel biotechnologiqueClostridium difficile (the novel name – Clostridioides difficile) is a Gram-positive, strictly anaerobic spore forming bacterium, found in soil and aquatic environments as well as in mammalian intestinal tracts. C. difficile is one of the major pathogenic clostridia. This bacterium has become a key public health issue associated with antibiotic therapy in industrialized countries. C. difficile-associated diarrhoea is currently the most frequently occurring nosocomial diarrhoea in Europe and worldwide. Since the last decade the number of severe infection forms has been rising due to emergence of the hypervirulent and epidemic strains as ribotype 027 R20291 strain. C. difficile infection causes diarrhoea, colitis and even death. Many aspects of C. difficile pathogenesis remain poorly understood. Particularly, the molecular mechanisms of its adaptation to changing conditions inside the host are to be scrutinized. During the infection cycle C. difficile survives in bacteriophage-rich gut communities possibly by relying on some special systems that control the genetic exchanges favored within these complex environments. During the last decade, CRISPR (clustered regularly interspaced short palindromic repeats)-Cas (CRISPR-associated) systems of adaptive prokaryotic immunity against exogenic genetic elements has become the center of interest among various anti-invader bacterial defense systems.Previous studies revealed the presence of abundant and diverse CRISPR RNAs in C. difficile. C. difficile has an original CRISPR system, which is characterized by the presence of an unusually large set of CRISPR arrays (12 arrays in the laboratory 630 strain and 9 ones in the hypervirulent R20291 strain), of two or three sets of cas genes conserved in the majority of sequenced C. difficile genomes and the prophage location of several CRISPR arrays. However, the role CRISPR-Cas plays in the physiology and infectious cycle of this important pathogen remains obscure.The general aims of this work run as follows: 1) to investigate the role and the functionality of C. difficile CRISPR-Cas system in the interactions with foreign DNA elements (such as plasmids), 2) to reveal the way C. difficile CRISPR-Cas system expression is regulated and functions in different states of bacterial culture, including its response to stresses. In the present PhD thesis the functionality of C. difficile CRISPR-Cas system was investigated (Chapter 2). Through conjugation efficiency assays defensive function (in interference) of C. difficile CRISPR-Cas system was demonstrated. The correlation between the previously known levels of expression of CRISPR RNAs and the observed levels of interference has also been shown. Moreover, through the series of interference experiments the functionality of PAMs (protospacer adjacent motifs) was confirmed, which have already been predicted in silico. Additionally, the general functional PAM consensus was determined using PAM libraries experiments. Furthermore, an adaptive function of C. difficile CRISPR-Cas system was shown for laboratory strain. The role of multiple cas operons in C. difficile CRISPR functionality is also demonstrated in this Chapter.In Chapter 3 the link between C. difficile CRISPR-Cas system and a new type I toxin-antitoxin system is demonstrated, as well as a possible co-regulation under biofilm and stress conditions of CRISPR-Cas system and these toxin-antitoxin modules. This Chapter also defines a possible role of c-di-GMP in regulation of C. difficile CRISPR-Cas system. Additionally, Chapter 4 describes the utilization of endogenous C. difficile CRISPR-Cas system as a novel tool for genome editing in C. difficile. Altogether, the obtained data highlight the original features of active C. difficile CRISPR-Cas system and demonstrate its biotechnological potential
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Thézé, Julien. "Diversification et adaptation génomique des virus entomopathogènes." Thesis, Tours, 2013. http://www.theses.fr/2013TOUR4006.
Abstract:
À différentes échelles de temps, le but de ma thèse a été de comprendre l'évolution des virus entomopathogènes à travers l’étude de la diversification et de l’adaptation génomique de grands virus à ADN d’insectes. Dans un premier temps, j’ai pu estimer les âges de diversifications des baculovirus et des nudivirus, et proposer un scénario de coévolution à long terme entre ces virus et leurs hôtes insectes. Puis, me plaçant sur une échelle de temps moindre, j’ai montré que les hôtes insectes sont le facteur principal de la diversification des baculovirus, et de façon surprenante, j’ai également observé que l'environnement biotique de ces virus, c’est-à-dire les plantes hôtes des insectes, joue un rôle central dans leur évolution. Dans un second temps, des mutations ponctuelles ont pu être reliées à l’adaptation locale de populations différentiées du baculovirus SeMNPV. Enfin, l’étude de l'adaptation génomique convergente entre les entomopoxvirus et les baculovirus a mis en évidence que les transferts horizontaux de gènes sont une source importante de variabilité pour les grands virus à ADN, pour l'adaptation aux mêmes niches écologiques. Les gènes et les mécanismes identifiés dans ce travail de thèse apportent des éléments nouveaux pour comprendre comment les génomes sont façonnés par l’écologieAt different timescales, the purpose of my PhD was to understand insect virus evolution through the study of the genomic diversification and adaptation of insect large DNA viruses. Firstly, I was able to estimate the ages of baculovirus and nudivirus diversifications, and to propose a long-term coevolutionary scenario between these viruses and their insect hosts. Then, on a narrower timescale, I showed that insect hosts are the major factor in baculovirus diversification, and surprisingly, I also observed that the virus biotic environment, i.e. insect host plants, plays a central role in their evolution. Secondly, punctual mutations have been linked to the local adaptation of differentiated populations of the baculovirus SeMNPV. Finally, the study of convergent genomic adaptation between entomopoxviruses and baculoviruses highlighted that horizontal gene transfers are an important source of variability for large DNA viruses, for the adaption to the same ecological niches. Genes and mechanisms identified in this PhD work provide new insights to understand how genomes are shaped by ecology
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Pawlik, Marie-Christin [Verfasser], and Ulrich [Akademischer Betreuer] Vogel. "Gene expression in the human pathogen Neisseria meningitidis: Adaptation to serum exposure and zinc limitation / Marie-Christin Pawlik. Betreuer: Ulrich Vogel." Würzburg : Universitätsbibliothek der Universität Würzburg, 2013. http://d-nb.info/1036836509/34.
Books on the topic "Pathogen adaptation":
1
Hsu, Ellen, and Louis Du Pasquier, eds. Pathogen-Host Interactions: Antigenic Variation v. Somatic Adaptations. Cham: Springer International Publishing, 2015. http://dx.doi.org/10.1007/978-3-319-20819-0.
2
1966-, Dieckmann Ulf, ed. Adaptive speciation. Cambridge, UK: Cambridge University Press, 2004.
3
Le May, Christophe, Josselin Montarry, Cindy E. Morris, Omer Frenkel, and Virginie Ravigné, eds. Plant Pathogen Life-History Traits and Adaptation to Environmental Constraints. Frontiers Media SA, 2020. http://dx.doi.org/10.3389/978-2-88963-530-6.
4
Griffiths, Mansel. Understanding Pathogen Behaviour: Virulence, Stress Response, and Resistance (Woodhead Publishing in Food Science and Technology). CRC Press, 2005.
5
Pasquier, Louis Du, and Ellen Hsu. Pathogen-Host Interactions: Antigenic Variation v. Somatic Adaptations. Springer, 2015.
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Pasquier, Louis Du, and Ellen Hsu. Pathogen-Host Interactions: Antigenic Variation V. Somatic Adaptations. Springer London, Limited, 2015.
7
Pasquier, Louis Du, and Ellen Hsu. Pathogen-Host Interactions: Antigenic Variation v. Somatic Adaptations. Springer, 2016.
8
Simões, Isaura, Daniel E. Voth, and Luís Jaime Mota, eds. Obligate Intracellular Bacteria: Evasion and Adaptative Tactics Shaping the Host-Pathogen Interface. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-753-3.
9
Brüne, Martin, and Wulf Schiefenhövel, eds. Oxford Handbook of Evolutionary Medicine. Oxford University Press, 2019. http://dx.doi.org/10.1093/oxfordhb/9780198789666.001.0001.
Abstract:
Medicine is grounded in the natural sciences, among which biology stands out with regard to the understanding of human physiology and conditions that cause dysfunction. Ironically, evolutionary biology is a relatively disregarded field. One reason for this omission is that evolution is deemed a slow process. Indeed, macroanatomical features of our species have changed very little in the last 300,000 years. A more detailed look, however, reveals that novel ecological contingencies, partly in relation to cultural evolution, have brought about subtle changes pertaining to metabolism and immunology, including adaptations to dietary innovations, as well as adaptations to exposure to novel pathogens. Rapid pathogen evolution and evolution of cancer cells cause major problems for the immune system to find adequate responses. Moreover, many adaptations to past ecologies have turned into risk factors for somatic disease and psychological disorder in our modern world (i.e. mismatch), among which epidemics of autoimmune diseases, cardiovascular diseases, diabetes, and obesity, as well as several forms of cancer stand out. In addition, depression, anxiety, and other psychiatric conditions add to the list. The Oxford Handbook of Evolutionary Medicine is a compilation of up-to-date insights into the evolutionary history of ourselves as a species, and how and why our evolved design may convey vulnerability to disease. Written in a classic textbook style, emphasising the physiology and pathophysiology of all major organ systems, the book addresses students as well as scholars in the fields of medicine, biology, anthropology, and psychology.
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Ahmed, Hafiz Uddin. Pathogenic variability and adaptation of Septoria tritici to different wheat cultivars. 1993.
Book chapters on the topic "Pathogen adaptation":
1
Heroven, Ann Kathrin, and Petra Dersch. "Metabolic Adaptation of Human PathogenicYersiniae." In Host - Pathogen Interaction, 1–18. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2016. http://dx.doi.org/10.1002/9783527682386.ch1.
2
Jagathjothi, N., M. Deivamani, M. Yuvaraj, R. Sathya Priya, M. Saranya, R. Sharmila, K. S. Subramanian, et al. "Plant Pathogen Mitigation and Adaptation to Climate Change." In Plant Quarantine Challenges under Climate Change Anxiety, 53–78. Cham: Springer Nature Switzerland, 2024. http://dx.doi.org/10.1007/978-3-031-56011-8_3.
3
de la Fuente, José, and Margarita Villar. "Conflict and cooperation in tick-host-pathogen interactions contribute to increased tick fitness and survival." In Climate, ticks and disease, 232–39. Wallingford: CABI, 2021. http://dx.doi.org/10.1079/9781789249637.0033.
Abstract:
Abstract This expert opinion discusses the mechanisms of tick-host-pathogen interactions and how these mediate the adaptation of tick species to climate change and hosts while guaranteeing completion of tick and pathogen life cycles as well as their impact on the prevalence of ticks and tick-borne diseases under climatic change events. A spotlight is given on the impact of Anaplasma phagocytophilum infection on tick and human cells as well as the relationship between conflict and cooperation of tick-host-pathogen interactions and climate change.
4
Kushwaha, Chanda, Neha Rani, and Arun P. Bhagat. "Chapter 13. Nature, Dissemination and Epidemiological Consequences in Charcoal Rot Pathogen Macrophomina Phaseolina." In The Phytopathogen Evolution and Adaptation, 357–80. 9 Spinnaker Way, Waretown, NJ 08758 USA: Apple Academic Press Inc., 2017. http://dx.doi.org/10.1201/9781315366135-17.
5
Bakshi, Suman, Johar Singh, and Sanjay J. Jambhulkar. "Isolation and characterization of yellow rust resistant mutants in wheat." In Mutation breeding, genetic diversity and crop adaptation to climate change, 103–10. Wallingford: CABI, 2021. http://dx.doi.org/10.1079/9781789249095.0010.
Abstract:
Abstract Stripe rust, also known as yellow rust, caused by Puccinia striiformis f. sp. tritici (Pst), is a major threat to wheat production leading to yield losses up to 84%. Due to climate change, new races of the yellow rust pathogen are appearing for which no durable source of resistance has been observed in the present high-yielding varieties. A mutation breeding programme was initiated in two popular varieties, namely PBW343 and HD2967, using gamma-ray and electron beam irradiation. Gamma-ray doses of 250, 300 and 350 Gy and electron beam doses of 150, 200 and 250 Gy were used for seed irradiation. The M2 population was screened in the field from seedling to adult plant stage by spraying a mixture of urediniospores of Pst pathotypes. Disease severity was recorded as the percentage of leaf area covered by the rust pathogen following a modified Cobb's scale. A total of 52 putative yellow rust resistant mutants in HD2967 and 63 in PBW343 were isolated. The number of mutants was higher in the electron beam irradiated population compared with gamma-rays. The absence of sporulation and spore production of the rust pathogen on the mutants indicated resistance. Mutant plants showing seedling resistance also showed resistance at adult plant stage. Seed yield and its contributing characters were better in the mutants compared with the parents. These rust resistant mutants could be novel sources of stripe rust or yellow rust resistance. The plant-to-row progenies of these mutants were confirmed and characterized in the M3 generation.
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Burdon, J. J. "Genetic Variation in Pathogen Populations and its Implications for Adaptation to Host Resistance." In Durability of Disease Resistance, 41–56. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-2004-3_4.
7
Ernst, Florian D., Arnoud H. M. van Vliet, Manfred Kist, Johannes G. Kusters, and Stefan Bereswill. "The Role of Nickel in Environmental Adaptation of the Gastric Pathogen Helicobacter pylori." In Nickel and Its Surprising Impact in Nature, 545–79. Chichester, UK: John Wiley & Sons, Ltd, 2007. http://dx.doi.org/10.1002/9780470028131.ch15.
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Pförtner, Henrike, Maren Depke, Kristin Surmann, Frank Schmidt, and Uwe Völker. "In vivo Proteomics Approaches for the Analysis of Bacterial Adaptation Reactions in Host–Pathogen Settings." In Methods in Molecular Biology, 207–28. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8695-8_15.
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Challa, Surekha, and Nageswara Rao Reddy Neelapu. "Association Between Horizontal Gene Transfer and Adaptation of Gastric Human Pathogen Helicobacter pylori to the Host." In Horizontal Gene Transfer, 257–67. Cham: Springer International Publishing, 2019. http://dx.doi.org/10.1007/978-3-030-21862-1_10.
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Epping, Lennard, Esther-Maria Antão, and Torsten Semmler. "Population Biology and Comparative Genomics of Campylobacter Species." In Current Topics in Microbiology and Immunology, 59–78. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-65481-8_3.
Abstract:
AbstractThe zoonotic pathogen Campylobacter is the leading cause for bacterial foodborne infections in humans. Campylobacters are most commonly transmitted via the consumption of undercooked poultry meat or raw milk products. The decreasing costs of whole genome sequencing enabled large genome-based analyses of the evolution and population structure of this pathogen, as well as the development of novel high-throughput molecular typing methods. Here, we review the evolutionary development and the population diversity of the two most clinically relevant Campylobacter species; C. jejuni and C. coli. The state-of-the-art phylogenetic studies showed clustering of C. jejuni lineages into host specialists and generalists with coexisting lifestyles in chicken and livestock-associated hosts, as well as the separation of C. coli isolates of riparian origin (waterfowl, water) from C. coli isolated from clinical and farm-related samples. We will give an overview of recombination between both species and the potential impact of horizontal gene transfer on host adaptation in Campylobacter. Additionally, this review briefly places the current knowledge of the population structure of other Campylobacter species such as C. lari, C. concisus and C. upsaliensis into perspective. We also provide an overview of how molecular typing methods such as multilocus sequence typing (MLST) and whole genome MLST have been used to detect and trace Campylobacter outbreaks along the food chain.
Conference papers on the topic "Pathogen adaptation":
1
Hulst, A. D., P. Bijma, and M. C. M. De Jong. "160. Can we prevent pathogen adaptation when breeding disease resistant livestock?" In World Congress on Genetics Applied to Livestock Production. The Netherlands: Wageningen Academic Publishers, 2022. http://dx.doi.org/10.3920/978-90-8686-940-4_160.
2
Yin, Chuntao. "Disease-induced changes in the rhizosphere microbiome reduced root disease." In IS-MPMI Congress. IS-MPMI, 2023. http://dx.doi.org/10.1094/ismpmi-2023-5r.
Abstract:
Rhizosphere microbiota, referred to as the second genome of plants, are crucial to plant health. Increasing evidence reveals that plants can change their rhizosphere microbiome and promote microbial activity to reduce plant disease. However, how plant and phytopathogens factor in combination to structure the rhizosphere microbiome and govern microbial selection for adaptation to disease stress remains incompletely understood. In this study, rhizosphere microbiota from successive wheat plantings under the pressure of the soilborne pathogen Rhizoctonia solani AG8 were characterized. Amplicon sequence analyses revealed that bacterial and fungal communities clustered by planting cycles. The addition of AG8 enhanced the separation of the rhizosphere microbiota. The alpha diversity of bacteria and fungi significantly decreased over planting cycles. Compared with rhizosphere bacterial communities, AG8 was a major driver structuring fungal communities. Pathogen-infected monocultures enriched a group of bacterial genera with potential antagonistic activities or abilities for plant growth promotion or nitrogen fixation. Further, eleven bacterial species exhibited antagonistic activities toward Rhizoctonia spp., and four of them displayed broad antagonism against multiple soilborne fungal pathogens. These findings support the potential to improve plant health through manipulating rhizosphere microbiota.
3
Bruun Jensen, Annette. "Fungal pathogen adaptations in social insects — Pandora’s Box." In 2016 International Congress of Entomology. Entomological Society of America, 2016. http://dx.doi.org/10.1603/ice.2016.92339.
4
Allen, Aideen C., Wladimir Malaga, Catherine Astarie-Dequeker, Ali Hassan, Céline Berrone, Flavie Moreau, Philip Supply, Roland Brosch, and Christophe Guilhot. "From environmental bacteria to obligate pathogen: the study of adaptations enhancing the persistence of tuberculosis bacilli." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.2802.
5
Allen, Aideen, Wladimir Malaga, Catherine Astarie-Dequeker, Ali Hassan, Céline Berrone, Flavie Moreau, Philip Supply, Roland Brosch, and Christophe Guilhot. "From environmental bacteria to obligate pathogen: the study of adaptations enhancing the persistence of tuberculosis bacilli." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4598.
6
MARSHALL, DAVID G., CHARLES J. DORMAN, FRANCES BOWE, CHRISTINE HALE, and GORDON DOUGAN. "DNA TOPOLOGY AND ADAPTATION OF SALMONELLA TYPHIMURIUM TO AN INTRACELLULAR ENVIRONMENT." In The Activities of Bacterial Pathogens in Vivo - Based on Contributions to a Royal Society Discussion Meeting. IMPERIAL COLLEGE PRESS, 2001. http://dx.doi.org/10.1142/9781848161610_0002.
Reports on the topic "Pathogen adaptation":
1
Melotto, M., and S. Sela. NIFA-BARD collaborative, mechanisms of salmonella adaptation to the lettuce phyllosphere. Israel: United States-Israel Binational Agricultural Research and Development Fund, 2022. http://dx.doi.org/10.32747/2022.8134153.bard.
Abstract:
The goal of this study is to evaluate the risk associated with colonization of the plant with Salmonella and to provide the scientific basis required to reduce plant's colonization by this pathogen through characterization of the molecular and physiological mechanisms that enable Salmonella to colonize vegetable crops
2
Eldar, Avigdor, and 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, December 2000. http://dx.doi.org/10.32747/2000.7575286.bard.
Abstract:
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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Sela, Shlomo, and Michael McClelland. Desiccation Tolerance in Salmonella and its Implications. United States Department of Agriculture, May 2013. http://dx.doi.org/10.32747/2013.7594389.bard.
Abstract:
Salmonella enterica is a worldwide food-borne pathogen, which regularly causes large outbreaks of food poisoning. Recent outbreaks linked to consumption of contaminated foods with low water-activity, have raised interest in understanding the factors that control fitness of this pathogen to dry environment. Consequently, the general objective of this study was to extend our knowledge on desiccation tolerance and long-term persistence of Salmonella. We discovered that dehydrated STm entered into a viable-but-nonculturable state, and that addition of chloramphenicol reduced bacterial survival. This finding implied that adaptation to desiccation stress requires de-novo protein synthesis. We also discovered that dried STm cells develop cross-tolerance to multiple stresses that the pathogen might encounter in the agriculture/food environment, such as high or low temperatures, salt, and various disinfectants. These findings have important implications for food safety because they demonstrate the limitations of chemical and physical treatments currently utilized by the food industry to completely inactivate Salmonella. In order to identify genes involved in desiccation stress tolerance, we employed transcriptomic analysis of dehydrated and wet cells and direct screening of knock-out mutant and transposon libraries. Transcriptomic analysis revealed that dehydration induced expression of ninety genes and down-regulated seven. Ribosomal structural genes represented the most abundant functional group with a relatively higher transcription during dehydration. Other large classes of induced functional groups included genes involved in amino acid metabolism, energy production, ion transport, transcription, and stress response. Initial genetic analysis of a number of up-regulated genes was carried out). It was found that mutations in rpoS, yahO, aceA, nifU, rpoE, ddg,fnr and kdpE significantly compromised desiccation tolerance, supporting their role in desiccation stress response.
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Freeman, Stanley, Russell Rodriguez, Adel Al-Abed, Roni Cohen, David Ezra, and Regina Redman. Use of fungal endophytes to increase cucurbit plant performance by conferring abiotic and biotic stress tolerance. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7613893.bard.
Abstract:
Major threats to agricultural sustainability in the 21st century are drought, increasing temperatures, soil salinity and soilborne pathogens, all of which are being exacerbated by climate change and pesticide abolition and are burning issues related to agriculture in the Middle East. We have found that Class 2 fungal endophytes adapt native plants to environmental stresses (drought, heat and salt) in a habitat-specific manner, and that these endophytes can confer stress tolerance to genetically distant monocot and eudicot hosts. In the past, we generated a uv non-pathogenic endophytic mutant of Colletotrichum magna (path-1) that colonized cucurbits, induced drought tolerance and enhanced growth, and protected 85% - 100% against disease caused by certain pathogenic fungi. We propose: 1) utilizing path-1 and additional endophtyic microorganisms to be isolated from stress-tolerant local, wild cucurbit watermelon, Citrulluscolocynthis, growing in the Dead Sea and Arava desert areas, 2) generate abiotic and biotic tolerant melon crop plants, colonized by the isolated endophytes, to increase crop yields under extreme environmental conditions such as salinity, heat and drought stress, 3) manage soilborne fungal pathogens affecting curubit crop species growing in the desert areas. This is a unique and novel "systems" approach that has the potential to utilize natural plant adaptation for agricultural development. We envisage that endophyte-colonized melons will eventually be used to overcome damages caused by soilborne diseases and also for cultivation of this crop, under stress conditions, utilizing treated waste water, thus dealing with the limited resource of fresh water.
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Shpigel, Nahum Y., Ynte Schukken, and Ilan Rosenshine. Identification of genes involved in virulence of Escherichia coli mastitis by signature tagged mutagenesis. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7699853.bard.
Abstract:
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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Splitter, Gary A., Menachem Banai, and Jerome S. Harms. Brucella second messenger coordinates stages of infection. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7699864.bard.
Abstract:
Aim 1: To determine levels of this second messenger in: a) B. melitensiscyclic-dimericguanosinemonophosphate-regulating mutants (BMEI1448, BMEI1453, and BMEI1520), and b) B. melitensis16M (wild type) and mutant infections of macrophages and immune competent mice. (US lab primary) Aim 2: To determine proteomic differences between Brucelladeletion mutants BMEI1453 (high cyclic-dimericguanosinemonophosphate, chronic persistent state) and BMEI1520 (low cyclicdimericguanosinemonophosphate, acute virulent state) compared to wild type B. melitensisto identify the role of this second messenger in establishing the two polar states of brucellosis. (US lab primary with synergistic assistance from the Israel lab Aim 3: Determine the level of Brucellacyclic-dimericguanosinemonophosphate and transcriptional expression from naturally infected placenta. (Israel lab primary with synergistic assistance from the US lab). B. Background Brucellaspecies are Gram-negative, facultative intracellular bacterial pathogens that cause brucellosis, the most prevalent zoonosis worldwide. Brucellosis is characterized by increased abortion, weak offspring, and decreased milk production in animals. Humans are infected with Brucellaby consuming contaminated milk products or via inhalation of aerosolized bacteria from occupational hazards. Chronic human infections can result in complications such as liver damage, orchitis, endocarditis, and arthritis. Brucellaspp. have the ability to infect both professional and non-professional phagocytes. Because of this, Brucellaencounter varied environments both throughout the body and within a cell and must adapt accordingly. To date, few virulence factors have been identified in B. melitensisand even less is known about how these virulence factors are regulated. Subsequently, little is known about how Brucellaadapt to its rapidly changing environments, and how it alternates between acute and chronic virulence. Our studies suggest that decreased concentrations of cyclic dimericguanosinemonophosphate (c-di-GMP) lead to an acute virulent state and increased concentrations of c-di-GMP lead to persistent, chronic state of B. melitensisin a mouse model of infection. We hypothesize that B. melitensisuses c-di-GMP to transition from the chronic state of an infected host to the acute, virulent stage of infection in the placenta where the bacteria prepare to infect a new host. Studies on environmental pathogens such as Vibrio choleraeand Pseudomonas aeruginosasupport a mechanism where changes in c-di-GMP levels cause the bacterium to alternate between virulent and chronic states. Little work exists on understanding the role of c-di-GMP in dangerous intracellular pathogens, like Brucellathat is a frequent pathogen in Israeli domestic animals and U.S. elk and bison. Brucellamust carefully regulate virulence factors during infection of a host to ensure proper expression at appropriate times in response to host cues. Recently, the novel secondary signaling molecule c-di-GMP has been identified as a major component of bacterial regulation and we have identified c-di-GMP as an important signaling factor in B. melitensishost adaptation. C. Major conclusions, solutions, achievements 1. The B. melitensis1453 deletion mutant has increased c-di-GMP, while the 1520 deletion mutant has decreased c-di-GMP. 2. Both mutants grow similarly in in vitro cultures; however, the 1453 mutant has a microcolony phenotype both in vitro and in vivo 3. The 1453 mutant has increased crystal violet staining suggesting biofilm formation. 4. Scanning electron microscopy revealed an abnormal coccus appearance with in increased cell area. 5. Proteomic analysis revealed the 1453 mutant possessed increased production of proteins involved in cell wall processes, cell division, and the Type IV secretion system, and a decrease in proteins involved in amino acid transport/metabolism, carbohydrate metabolism, fatty acid production, and iron acquisition suggesting less preparedness for intracellular survival. 6. RNAseq analysis of bone marrow derived macrophages infected with the mutants revealed the host immune response is greatly reduced with the 1453 mutant infection. These findings support that microlocalization of proteins involved in c-di-GMP homeostasis serve a second messenger to B. melitensisregulating functions of the bacteria during infection of the host.
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Sela, Hanan, Eduard Akhunov, and Brian J. Steffenson. Population genomics, linkage disequilibrium and association mapping of stripe rust resistance genes in wild emmer wheat, Triticum turgidum ssp. dicoccoides. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598170.bard.
Abstract:
The primary goals of this project were: (1) development of a genetically characterized association panel of wild emmer for high resolution analysis of the genetic basis of complex traits; (2) characterization and mapping of genes and QTL for seedling and adult plant resistance to stripe rust in wild emmer populations; (3) characterization of LD patterns along wild emmer chromosomes; (4) elucidation of the multi-locus genetic structure of wild emmer populations and its correlation with geo-climatic variables at the collection sites. Introduction In recent years, Stripe (yellow) rust (Yr) caused by Pucciniastriiformis f. sp. tritici(PST) has become a major threat to wheat crops in many parts of the world. New races have overcome most of the known resistances. It is essential, therefore, that the search for new genes will continue, followed by their mapping by molecular markers and introgression into the elite varieties by marker-assisted selection (MAS). The reservoir of genes for disease and pest resistance in wild emmer wheat (Triticumdicoccoides) is an important resource that must be made available to wheat breeders. The majority of resistance genes that were introgressed so far in cultivated wheat are resistance (R) genes. These genes, though confering near-immunity from the seedling stage, are often overcome by the pathogen in a short period after being deployed over vast production areas. On the other hand, adult-plant resistance (APR) is usually more durable since it is, in many cases, polygenic and confers partial resistance that may put less selective pressure on the pathogen. In this project, we have screened a collection of 480 wild emmer accessions originating from Israel for APR and seedling resistance to PST. Seedling resistance was tested against one Israeli and 3 North American PST isolates. APR was tested on accessions that did not have seedling resistance. The APR screen was conducted in two fields in Israel and in one field in the USA over 3 years for a total of 11 replicates. We have found about 20 accessions that have moderate stripe rust APR with infection type (IT<5), and about 20 additional accessions that have novel seedling resistance (IT<3). We have genotyped the collection using genotyping by sequencing (GBS) and the 90K SNP chip array. GBS yielded a total 341K SNP that were filtered to 150K informative SNP. The 90K assay resulted in 11K informative SNP. We have conducted a genome-wide association scan (GWAS) and found one significant locus on 6BL ( -log p >5). Two novel loci were found for seedling resistance. Further investigation of the 6BL locus and the effect of Yr36 showed that the 6BL locus and the Yr36 have additive effect and that the presence of favorable alleles of both loci results in reduction of 2 grades in the IT score. To identify alleles conferring adaption to extreme climatic conditions, we have associated the patterns of genomic variation in wild emmer with historic climate data from the accessions’ collection sites. The analysis of population stratification revealed four genetically distinct groups of wild emmer accessions coinciding with their geographic distribution. Partitioning of genomic variance showed that geographic location and climate together explain 43% of SNPs among emmer accessions with 19% of SNPs affected by climatic factors. The top three bioclimatic factors driving SNP distribution were temperature seasonality, precipitation seasonality, and isothermality. Association mapping approaches revealed 57 SNPs associated with these bio-climatic variables. Out of 21 unique genomic regions controlling heading date variation, 10 (~50%) overlapped with SNPs showing significant association with at least one of the three bioclimatic variables. This result suggests that a substantial part of the genomic variation associated with local adaptation in wild emmer is driven by selection acting on loci regulating flowering. Conclusions: Wild emmer can serve as a good source for novel APR and seedling R genes for stripe rust resistance. APR for stripe rust is a complex trait conferred by several loci that may have an additive effect. GWAS is feasible in the wild emmer population, however, its detection power is limited. A panel of wild emmer tagged with more than 150K SNP is available for further GWAS of important traits. The insights gained by the bioclimatic-gentic associations should be taken into consideration when planning conservation strategies.
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Porat, Ron, Gregory T. McCollum, Amnon Lers, and Charles L. Guy. Identification and characterization of genes involved in the acquisition of chilling tolerance in citrus fruit. United States Department of Agriculture, December 2007. http://dx.doi.org/10.32747/2007.7587727.bard.
Abstract:
Citrus, like many other tropical and subtropical fruit are sensitive to chilling temperatures. However, application of a pre-storage temperature conditioning (CD) treatment at 16°C for 7 d or of a hot water brushing (HWB) treatment at 60°C for 20 sec remarkably enhances chilling tolerance and reduces the development of chilling injuries (CI) upon storage at 5°C. In the current research, we proposed to identify and characterize grapefruit genes that are induced by CD, and may contribute to the acquisition of fruit chilling tolerance, by two different molecular approaches: cDNA array analysis and PCR cDNA subtraction. In addition, following the recent development and commercialization of the new Affymetrix Citrus Genome Array, we further performed genome-wide transcript profiling analysis following exposure to CD and chilling treatments. To conduct the cDNA array analysis, we constructed cDNA libraries from the peel tissue of CD- and HWB-treated grapefruit, and performed an EST sequencing project including sequencing of 3,456 cDNAs from each library. Based on the obtained sequence information, we chose 70 stress-responsive and chilling-related genes and spotted them on nylon membranes. Following hybridization the constructed cDNA arrays with RNA probes from control and CD-treated fruit and detailed confirmations by RT-PCR analysis, we found that six genes: lipid-transfer protein, metallothionein-like protein, catalase, GTP-binding protein, Lea5, and stress-responsive zinc finger protein, showed higher transcript levels in flavedo of conditioned than in non-conditioned fruit stored at 5 ᵒC. The transcript levels of another four genes: galactinol synthase, ACC oxidase, temperature-induced lipocalin, and chilling-inducible oxygenase, increased only in control untreated fruit but not in chilling-tolerant CD-treated fruit. By PCR cDNA subtraction analysis we identified 17 new chilling-responsive and HWB- and CD-induced genes. Overall, characterization of the expression patterns of these genes as well as of 11 more stress-related genes by RNA gel blot hybridizations revealed that the HWB treatment activated mainly the expression of stress-related genes(HSP19-I, HSP19-II, dehydrin, universal stress protein, EIN2, 1,3;4-β-D-glucanase, and SOD), whereas the CD treatment activated mainly the expression of lipid modification enzymes, including fatty acid disaturase2 (FAD2) and lipid transfer protein (LTP). Genome wide transcriptional profiling analysis using the newly developed Affymetrix Citrus GeneChip® microarray (including 30,171 citrus probe sets) revealed the identification of three different chilling-related regulons: 1,345 probe sets were significantly affected by chilling in both control and CD-treated fruits (chilling-response regulon), 509 probe sets were unique to the CD-treated fruits (chilling tolerance regulon), and 417 probe sets were unique to the chilling-sensitive control fruits (chilling stress regulon). Overall, exposure to chilling led to expression governed arrest of general cellular metabolic activity, including concretive down-regulation of cell wall, pathogen defense, photosynthesis, respiration, and protein, nucleic acid and secondary metabolism. On the other hand, chilling enhanced various adaptation processes, such as changes in the expression levels of transcripts related to membranes, lipid, sterol and carbohydrate metabolism, stress stimuli, hormone biosynthesis, and modifications in DNA binding and transcription factors.
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Chiel, Elad, and Christopher J. Geden. Development of sustainable fly management tools in an era of global warming. United States Department of Agriculture, January 2014. http://dx.doi.org/10.32747/2014.7598161.bard.
Abstract:
House flies (Muscadomestica) are global pests of animal agriculture, causing major annoyance, carrying pathogens among production facilities and humans and thus have profound impacts on animal comfort and productivity. Successful fly control requires an integrated pest management (IPM) approach that includes elements of manure management, mass trapping, biological control, and selective insecticide use. Insecticidal control of house flies has become increasingly difficult due to the rapidity with which resistance develops, even to new active ingredients. Global climate change poses additional challenges, as the efficacy of natural enemies is uncertain under the higher temperatures that are predicted to become more commonplace in the future. The two major objectives of this research project were: 1) to develop a cost-effective autodissemination application method of Pyriproxifen (PPF), an insect growth regulator, for controlling house flies; 2) to study the effect of increasing temperatures on the interactions between house flies and their principal natural enemies. First, we collected several wild house fly populations in both countries and established that most of them are susceptible to PPF, although one population in each country showed initial signs of PPF-resistance. An important finding is that the efficacy of PPF is substantially reduced when applied in cows’ manure. We also found that PPF is compatible with several common species of parasitoids that attack the house fly, thus PPF can be used in IPM programs. Next, we tried to develop “baited stations” in which house flies will collect PPF on their bodies and then deliver and deposit it in their oviposition sites (= autodissemination). The concept showed potential in lab experiments and in outdoor cages trials, but under field conditions the station models we tested were not effective enough. We thus tested a somewhat different approach – to actively release a small proportion of PPF-treated flies. This approach showed positive results in laboratory experiments and awaits further field experiments. On the second topic, we performed two experimental sets: 1) we collected house flies and their parasitoids from hot temperature and mild temperature areas in both countries and, by measuring some fitness parameters we tested whether the ones collected from hot areas are better adapted to BARD Report - Project 4701 Page 2 of 16 heat. The results showed very little differences between the populations, both of flies and parasitoids. 2) A “fast evolution” experiment, in which we reared house flies for 20 generations under increasing temperatures. Also here, we found no evidence for heat adaptation. In summary, pyriproxyfen proved to be a highly effective insect growth regulator for house flies that is compatible with it’s natural enemies. Although our autodissemination stations yielded disappointing results, we documented the proportion of flies in a population that must be exposed to PPF to achieve effective fly control. Both the flies and their principal parasitoids show no evidence for local adaptation to high temperatures. This is an encouraging finding for biological control, as our hypothesis was that the fly would be adapting faster to high temperatures than the parasitoids. BARD Report - Project 4701 Page 3 of 16