Articoli di riviste: "Pathogen adaptation"

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Fonville, Judith M. "Expected Effect of Deleterious Mutations on Within-Host Adaptation of Pathogens". Journal of Virology 89, n. 18 (24 giugno 2015): 9242–51. http://dx.doi.org/10.1128/jvi.00832-15.

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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 e Daniel Croll. "The Genome Biology of Effector Gene Evolution in Filamentous Plant Pathogens". Annual Review of Phytopathology 56, n. 1 (25 agosto 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, n. 6517 (5 novembre 2020): 677.20–679. http://dx.doi.org/10.1126/science.370.6517.677-t.

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Slev, Patricia R., e Wayne K. Potts. "Disease consequences of pathogen adaptation". Current Opinion in Immunology 14, n. 5 (ottobre 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 e Peter H. Thrall. "Host ecotype generates evolutionary and epidemiological divergence across a pathogen metapopulation". Proceedings of the Royal Society B: Biological Sciences 281, n. 1787 (22 luglio 2014): 20140522. http://dx.doi.org/10.1098/rspb.2014.0522.

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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 e Yousef Abu Kwaik. "Bacterial nucleomodulins: A coevolutionary adaptation to the eukaryotic command center". PLOS Pathogens 17, n. 1 (21 gennaio 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 e Valerio Napolioni. "Genetic adaptation to historical pathogen burdens". Infection, Genetics and Evolution 54 (ottobre 2017): 299–307. http://dx.doi.org/10.1016/j.meegid.2017.07.017.

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TASARA, T., e R. STEPHAN. "Cold Stress Tolerance of Listeria monocytogenes: A Review of Molecular Adaptive Mechanisms and Food Safety Implications". Journal of Food Protection 69, n. 6 (1 giugno 2006): 1473–84. http://dx.doi.org/10.4315/0362-028x-69.6.1473.

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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 e James S. Adelman. "Rapid adaptation to a novel pathogen through disease tolerance in a wild songbird". PLOS Pathogens 19, n. 6 (9 giugno 2023): e1011408. http://dx.doi.org/10.1371/journal.ppat.1011408.

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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, n. 3 (15 ottobre 2021): 856–67. http://dx.doi.org/10.1038/s41396-021-01134-2.

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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.

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Bidochka, Michael J., Susan Burke e Luna Ng. "Extracellular hydrolytic enzymes in the fungal genus Verticillium: adaptations for pathogenesis". Canadian Journal of Microbiology 45, n. 10 (1 ottobre 1999): 856–64. http://dx.doi.org/10.1139/w99-085.

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The insect and plant pathogens within the fungal genus Verticillium showed enzymatic adaptation (production and regulation) directed to the degradation of some of the polymers found in the integument of their respective hosts. For example, the facultative plant pathogens (V. albo-atrum and V. dahliae) produced greater levels of cellulase and xylanase than the facultative insect pathogen (V. lecanii). Verticillium lecanii produced extracellular subtilisin-like protease when grown in insect cuticle medium but not in plant cell wall medium, while the plant pathogen V. albo-atrum showed a diminished regulatory component in the production of this enzyme. The opportunistic pathogens (V. fungicola and V. coccosporum) and the saprobic species (V. rexianum) were less specific in the production and regulation of several proteases as well as cellulases and xylanases. A dendrogram based on cluster analysis compiled from fungal API-ZYM profiles showed commonalties in a broad array of extracellular enzymes within a host-pathogen group (i.e. insect or plant pathogen). The opportunistic pathogens were dispersed throughout the dendrogram, suggestive of the diversity in type and expression of extracellular enzymes.Key words: extracellular enzymes, pathogenic fungi.

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Wu, E.-Jiao, Yan-Ping Wang, Li-Na Yang, Mi-Zhen Zhao e Jiasui Zhan. "Elevating Air Temperature may Enhance Future Epidemic Risk of the Plant Pathogen Phytophthora infestans". Journal of Fungi 8, n. 8 (30 luglio 2022): 808. http://dx.doi.org/10.3390/jof8080808.

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Knowledge of pathogen adaptation to global warming is important for predicting future disease epidemics and food production in agricultural ecosystems; however, the patterns and mechanisms of such adaptation in many plant pathogens are poorly understood. Here, population genetics combined with physiological assays and common garden experiments were used to analyze the genetics, physiology, and thermal preference of pathogen aggressiveness in an evolutionary context using 140 Phytophthora infestans genotypes under five temperature regimes. Pathogens originating from warmer regions were more thermophilic and had a broader thermal niche than those from cooler regions. Phenotypic plasticity contributed ~10-fold more than heritability measured by genetic variance. Further, experimental temperatures altered the expression of genetic variation and the association of pathogen aggressiveness with the local temperature. Increasing experimental temperature enhanced the variation in aggressiveness. At low experimental temperatures, pathogens from warmer places produced less disease than those from cooler places; however, this pattern was reversed at higher experimental temperatures. These results suggest that geographic variation in the thermal preferences of pathogens should be included in modeling future disease epidemics in agricultural ecosystems in response to global warming, and greater attention should be paid to preventing the movement of pathogens from warmer to cooler places.

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Mayer, Andreas, Thierry Mora, Olivier Rivoire e Aleksandra M. Walczak. "Diversity of immune strategies explained by adaptation to pathogen statistics". Proceedings of the National Academy of Sciences 113, n. 31 (18 luglio 2016): 8630–35. http://dx.doi.org/10.1073/pnas.1600663113.

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Biological organisms have evolved a wide range of immune mechanisms to defend themselves against pathogens. Beyond molecular details, these mechanisms differ in how protection is acquired, processed, and passed on to subsequent generations—differences that may be essential to long-term survival. Here, we introduce a mathematical framework to compare the long-term adaptation of populations as a function of the pathogen dynamics that they experience and of the immune strategy that they adopt. We find that the two key determinants of an optimal immune strategy are the frequency and the characteristic timescale of the pathogens. Depending on these two parameters, our framework identifies distinct modes of immunity, including adaptive, innate, bet-hedging, and CRISPR-like immunities, which recapitulate the diversity of natural immune systems.

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Dutta, Anik, Fanny E. Hartmann, Carolina Sardinha Francisco, Bruce A. McDonald e Daniel Croll. "Mapping the adaptive landscape of a major agricultural pathogen reveals evolutionary constraints across heterogeneous environments". ISME Journal 15, n. 5 (15 gennaio 2021): 1402–19. http://dx.doi.org/10.1038/s41396-020-00859-w.

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AbstractThe adaptive potential of pathogens in novel or heterogeneous environments underpins the risk of disease epidemics. Antagonistic pleiotropy or differential resource allocation among life-history traits can constrain pathogen adaptation. However, we lack understanding of how the genetic architecture of individual traits can generate trade-offs. Here, we report a large-scale study based on 145 global strains of the fungal wheat pathogen Zymoseptoria tritici from four continents. We measured 50 life-history traits, including virulence and reproduction on 12 different wheat hosts and growth responses to several abiotic stressors. To elucidate the genetic basis of adaptation, we used genome-wide association mapping coupled with genetic correlation analyses. We show that most traits are governed by polygenic architectures and are highly heritable suggesting that adaptation proceeds mainly through allele frequency shifts at many loci. We identified negative genetic correlations among traits related to host colonization and survival in stressful environments. Such genetic constraints indicate that pleiotropic effects could limit the pathogen’s ability to cause host damage. In contrast, adaptation to abiotic stress factors was likely facilitated by synergistic pleiotropy. Our study illustrates how comprehensive mapping of life-history trait architectures across diverse environments allows to predict evolutionary trajectories of pathogens confronted with environmental perturbations.

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Lloyd-Smith, James O. "Vacated niches, competitive release and the community ecology of pathogen eradication". Philosophical Transactions of the Royal Society B: Biological Sciences 368, n. 1623 (5 agosto 2013): 20120150. http://dx.doi.org/10.1098/rstb.2012.0150.

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A recurring theme in the epidemiological literature on disease eradication is that each pathogen occupies an ecological niche, and eradication of one pathogen leaves a vacant niche that favours the emergence of new pathogens to replace it. However, eminent figures have rejected this view unequivocally, stating that there is no basis to fear pathogen replacement and even that pathogen niches do not exist. After exploring the roots of this controversy, I propose resolutions to disputed issues by drawing on broader ecological theory, and advance a new consensus based on robust mechanistic principles. I argue that pathogen eradication (and cessation of vaccination) leads to a ‘vacated niche’, which could be re-invaded by the original pathogen if introduced. Consequences for other pathogens will vary, with the crucial mechanisms being competitive release, whereby the decline of one species allows its competitors to perform better, and evolutionary adaptation. Hence, eradication can cause a quantitative rise in the incidence of another infection, but whether this leads to emergence as an endemic pathogen depends on additional factors. I focus on the case study of human monkeypox and its rise following smallpox eradication, but also survey how these ideas apply to other pathogens and discuss implications for eradication policy.

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Råberg, Lars. "Human and pathogen genotype-by-genotype interactions in the light of coevolution theory". PLOS Genetics 19, n. 4 (6 aprile 2023): e1010685. http://dx.doi.org/10.1371/journal.pgen.1010685.

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Antagonistic coevolution (i.e., reciprocal adaptation and counter-adaptation) between hosts and pathogens has long been considered an important driver of genetic variation. However, direct evidence for this is still scarce, especially in vertebrates. The wealth of data on genetics of susceptibility to infectious disease in humans provides an important resource for understanding host–pathogen coevolution, but studies of humans are rarely framed in coevolutionary theory. Here, I review data from human host–pathogen systems to critically assess the evidence for a key assumption of models of host–pathogen coevolution—the presence of host genotype-by-pathogen genotype interactions (G×G). I also attempt to infer whether observed G×G fit best with “gene-for-gene” or “matching allele” models of coevolution. I find that there are several examples of G×G in humans (involving, e.g., ABO, HBB, FUT2, SLC11A1, and HLA genes) that fit assumptions of either gene-for-gene or matching allele models. This means that there is potential for coevolution to drive polymorphism also in humans (and presumably other vertebrates), but further studies are required to investigate how widespread this process is.

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Cory, Jenny S., e Judith H. Myers. "Adaptation in an insect host-plant pathogen interaction". Ecology Letters 7, n. 8 (agosto 2004): 632–39. http://dx.doi.org/10.1111/j.1461-0248.2004.00617.x.

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Koelle, Katia, Mercedes Pascual e Md Yunus. "Pathogen adaptation to seasonal forcing and climate change". Proceedings of the Royal Society B: Biological Sciences 272, n. 1566 (7 maggio 2005): 971–77. http://dx.doi.org/10.1098/rspb.2004.3043.

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van Boven, Michiel, Frits R. Mooi, Joop F. P. Schellekens, Hester E. de Melker e Mirjam Kretzschmar. "Pathogen adaptation under imperfect vaccination: implications for pertussis". Proceedings of the Royal Society B: Biological Sciences 272, n. 1572 (6 luglio 2005): 1617–24. http://dx.doi.org/10.1098/rspb.2005.3108.

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Mass vaccination campaigns have drastically reduced the burden of infectious diseases. Unfortunately, in recent years several infectious diseases have re-emerged. Pertussis poses a well-known example. Inspired by pertussis, we study, by means of an epidemic model, the population and evolutionary dynamics of a pathogen population under the pressure of vaccination. A distinction is made between infection in immunologically naive individuals (primary infection) and infection in individuals whose immune system has been primed by vaccination or infection (secondary infection). The results show that (i) vaccination with an imperfect vaccine may not succeed in reducing the infection pressure if the transmissibility of secondary infections is higher than that of primary infections; (ii) pathogen strains that are able to evade the immunity induced by vaccination can only spread if escape mutants incur no or only a modest fitness cost and (iii) the direction of evolution depends crucially on the distribution of the different types of susceptibles in the population. We discuss the implications of these results for the design and use of vaccines that provide temporary immunity.

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Bourget, Romain, Loïc Chaumont e Natalia Sapoukhina. "Timing of Pathogen Adaptation to a Multicomponent Treatment". PLoS ONE 8, n. 8 (21 agosto 2013): e71926. http://dx.doi.org/10.1371/journal.pone.0071926.

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Harkins, Kelly M., e Anne C. Stone. "Ancient pathogen genomics: insights into timing and adaptation". Journal of Human Evolution 79 (febbraio 2015): 137–49. http://dx.doi.org/10.1016/j.jhevol.2014.11.002.

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ZHAN, JIASUI, e BRUCE A. McDONALD. "Thermal adaptation in the fungal pathogen Mycosphaerella graminicola". Molecular Ecology 20, n. 8 (14 marzo 2011): 1689–701. http://dx.doi.org/10.1111/j.1365-294x.2011.05023.x.

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Langridge, Gemma C., Maria Fookes, Thomas R. Connor, Theresa Feltwell, Nicholas Feasey, Bryony N. Parsons, Helena M. B. Seth-Smith et al. "Patterns of genome evolution that have accompanied host adaptation inSalmonella". Proceedings of the National Academy of Sciences 112, n. 3 (22 dicembre 2014): 863–68. http://dx.doi.org/10.1073/pnas.1416707112.

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Many bacterial pathogens are specialized, infecting one or few hosts, and this is often associated with more acute disease presentation. Specific genomes show markers of this specialization, which often reflect a balance between gene acquisition and functional gene loss. WithinSalmonella entericasubspeciesenterica, a single lineage exists that includes human and animal pathogens adapted to cause infection in different hosts, includingS. entericaserovar Enteritidis (multiple hosts),S.Gallinarum (birds), andS.Dublin (cattle). This provides an excellent evolutionary context in which differences between these pathogen genomes can be related to host range. Genome sequences were obtained from ∼60 isolates selected to represent the known diversity of this lineage. Examination and comparison of the clades within the phylogeny of this lineage revealed signs of host restriction as well as evolutionary events that mark a path to host generalism. We have identified the nature and order of events for both evolutionary trajectories. The impact of functional gene loss was predicted based upon position within metabolic pathways and confirmed with phenotyping assays. The structure ofS.Enteritidis is more complex than previously known, as a second clade ofS.Enteritidis was revealed that is distinct from those commonly seen to cause disease in humans or animals, and that is more closely related toS.Gallinarum. Isolates from this second clade were tested in a chick model of infection and exhibited a reduced colonization phenotype, which we postulate represents an intermediate stage in pathogen–host adaptation.

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Wang, Liyuan, Han Chen, JiangJiang Li, Haidong Shu, Xiangxue Zhang, Yuanchao Wang, Brett M. Tyler e Suomeng Dong. "Effector gene silencing mediated by histone methylation underpins host adaptation in an oomycete plant pathogen". Nucleic Acids Research 48, n. 4 (10 dicembre 2019): 1790–99. http://dx.doi.org/10.1093/nar/gkz1160.

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Abstract The relentless adaptability of pathogen populations is a major obstacle to effective disease control measures. Increasing evidence suggests that gene transcriptional polymorphisms are a strategy deployed by pathogens to evade host immunity. However, the underlying mechanisms of transcriptional plasticity remain largely elusive. Here we found that the soybean root rot pathogen Phytophthora sojae evades the soybean Resistance gene Rps1b through transcriptional polymorphisms in the effector gene Avr1b that occur in the absence of any sequence variation. Elevated levels of histone H3 Lysine27 tri-methylation (H3K27me3) were observed at the Avr1b locus in a naturally occurring Avr1b-silenced strain but not in an Avr1b-expressing strain, suggesting a correlation between this epigenetic modification and silencing of Avr1b. To genetically test this hypothesis, we edited the gene, PsSu(z)12, encoding a core subunit of the H3K27me3 methyltransferase complex by using CRISPR/Cas9, and obtained three deletion mutants. H3K27me3 depletion within the Avr1b genomic region correlated with impaired Avr1b gene silencing in these mutants. Importantly, these mutants lost the ability to evade immune recognition by soybeans carrying Rps1b. These data support a model in which pathogen effector transcriptional polymorphisms are associated with changes in chromatin epigenetic marks, highlighting epigenetic variation as a mechanism of pathogen adaptive plasticity.

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Sacristán, Soledad, Aurora Fraile, José M. Malpica e Fernando García-Arenal. "An Analysis of Host Adaptation and Its Relationship with Virulence in Cucumber mosaic virus". Phytopathology® 95, n. 7 (luglio 2005): 827–33. http://dx.doi.org/10.1094/phyto-95-0827.

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The host range of a pathogen can have special consequences on its evolution and the evolution of its virulence. For generalists, adaptation to different hosts may be conditioned by different trade-offs in the pathogen's life history and be affected by evolutionary processes that shape pathogen populations. We have examined adaptation of Cucumber mosaic virus (CMV) to different hosts, and analyzed the relationship between host adaptation and virulence. For this, six CMV isolates from central Spain from three different hosts were compared for the ability to multiply and to affect host growth. These analyses were done before and after an experimental evolution process consisting of 10 serial passages in the original host of the isolate. The differential capacity to infect different hosts was compatible with host adaptation. However, the capacity to multiply in different hosts did not provide evidence of host adaptation and was not improved after 10 passages, suggesting that fitness of the natural population of CMV was at, or near to, its maximum. No relationship was found between capacity of multiplication and virulence in any of the three different hosts. These results suggest that the “trade-off” model for the evolution of virulence may not apply to CMV.

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Dawidziuk, A., G. Koczyk e D. Popiel. "Adaptation and response to mycotoxin presence in pathogen-pathogen interactions within the Fusarium genus". World Mycotoxin Journal 9, n. 4 (24 ottobre 2016): 565–75. http://dx.doi.org/10.3920/wmj2015.2010.

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The ability of fungal plant pathogens to exude bioactive compounds is an important element of competition in a changing environment. The filamentous fungi usually retain a number of adaptations related not only to the production of toxic compounds by themselves but also to the mitigation of exogenous influences by toxins present in the environment. We examined a distinct effect of toxins on morphology, growth patterns and gene expression after stimulation in mycotoxin-producing and nonproducing isolates representing four evolutionarily divergent species (and chemotypes) within the Fusarium genus (Fusarium graminearum, Fusarium oxysporum, Fusarium proliferatum and Fusarium verticillioides). The aim of our work was to investigate the influence of mycotoxins present in the environment on fungal isolates belonging to evolutionarily divergent complexes within Fusarium genus. The results point to retention of resistance mechanisms in non-producer isolates (F. oxysporum) and specific dose-dependent differences in response to other mycotoxins. In particular, the growth of Fusarium graminearum (confirmed zearalenone and trichothecene producer) was shown to be significantly inhibited by fumonisin B1 and deoxynivalenol. Conversely, spread of Fusarium verticillioides was accelerated by low concentrations (0.5 mg/l) of nivalenol and zearalenone and deoxynivalenol addition resulted in upregulation of the fumonisin poliketyde synthase (FUM1). The basics of competition between divergent fusaria can be described by ‘rock-paper-scissors’ theory, but some of the effects can be explained by other interactions, e.g. autotoxicity of deoxynivalenol and the potential role of low doses of trichothecenes and zearalenone acting as a ‘warning signal’ for competing species.

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Précigout, Pierre-Antoine, Corinne Robert e David Claessen. "Adaptation of Biotrophic Leaf Pathogens to Fertilization-Mediated Changes in Plant Traits: A Comparison of the Optimization Principle to Invasion Fitness". Phytopathology® 110, n. 5 (maggio 2020): 1039–48. http://dx.doi.org/10.1094/phyto-08-19-0317-r.

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One of the conclusions of evolutionary ecology applied to agroecosystem management is that sustainable disease management strategies must be adaptive to overcome the immense adaptive potential of crop pathogens. In this context, knowledge of how pathogens adapt to changes in cultural practices is necessary. In this article we address the issue of the evolutionary response of biotrophic crop pathogens to changes in fertilization practices. For this purpose, we compare predictions of latent period evolution based on three empirical fitness measures (seasonal spore production, within-season exponential growth rate, and area under disease progress curves [AUDPCs]) with predictions based on the concept of invasion fitness from adaptive dynamics. We use pairwise invisibility plots to identify the evolutionarily stable strategies (ESSs) of the pathogen latent period. We find that the ESS latent period is in between the latent periods that maximize the seasonal spore production and the within-season exponential growth rate of the pathogen. The latent periods that maximize the AUDPC are similar to those of the ESS latent periods. The AUDPC may therefore be a critical variable to determine the issue of between-strain competition and shape pathogen evolution.

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Baxter, Laura, Sucheta Tripathy, Naveed Ishaque, Nico Boot, Adriana Cabral, Eric Kemen, Marco Thines et al. "Signatures of Adaptation to Obligate Biotrophy in the Hyaloperonospora arabidopsidis Genome". Science 330, n. 6010 (9 dicembre 2010): 1549–51. http://dx.doi.org/10.1126/science.1195203.

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Many oomycete and fungal plant pathogens are obligate biotrophs, which extract nutrients only from living plant tissue and cannot grow apart from their hosts. Although these pathogens cause substantial crop losses, little is known about the molecular basis or evolution of obligate biotrophy. Here, we report the genome sequence of the oomycete Hyaloperonospora arabidopsidis (Hpa), an obligate biotroph and natural pathogen of Arabidopsis thaliana. In comparison with genomes of related, hemibiotrophic Phytophthora species, the Hpa genome exhibits dramatic reductions in genes encoding (i) RXLR effectors and other secreted pathogenicity proteins, (ii) enzymes for assimilation of inorganic nitrogen and sulfur, and (iii) proteins associated with zoospore formation and motility. These attributes comprise a genomic signature of evolution toward obligate biotrophy.

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Goel, Ajay K., Derek Lundberg, Miguel A. Torres, Ryan Matthews, Chiharu Akimoto-Tomiyama, Lisa Farmer, Jeffery L. Dangl e Sarah R. Grant. "The Pseudomonas syringae Type III Effector HopAM1 Enhances Virulence on Water-Stressed Plants". Molecular Plant-Microbe Interactions® 21, n. 3 (marzo 2008): 361–70. http://dx.doi.org/10.1094/mpmi-21-3-0361.

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Pseudomonas syringae strains deliver diverse type III effector proteins into host cells, where they can act as virulence factors. Although the functions of the majority of type III effectors are unknown, several have been shown to interfere with plant basal defense mechanisms. Type III effectors also could contribute to bacterial virulence by enhancing nutrient uptake and pathogen adaptation to the environment of the host plant. We demonstrate that the type III effector HopAM1 (formerly known as AvrPpiB) enhances the virulence of a weak pathogen in plants that are grown under drought stress. This is the first report of a type III effector that aids pathogen adaptation to water availability in the host plant. Expression of HopAM1 makes transgenic Ws-0 Arabidopsis hypersensitive to abscisic acid (ABA) for stomatal closure and germination arrest. Conditional expression of HopAM1 in Arabidopsis also suppresses basal defenses. ABA responses overlap with defense responses and ABA has been shown to suppress defense against P. syringae pathogens. We propose that HopAM1 aids P. syringae virulence by manipulation of ABA responses that suppress defense responses. In addition, host ABA responses enhanced by type III delivery of HopAM1 protect developing bacterial colonies inside leaves from osmotic stress.

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Keon, John, John Antoniw, Raffaella Carzaniga, Siân Deller, Jane L. Ward, John M. Baker, Michael H. Beale, Kim Hammond-Kosack e Jason J. Rudd. "Transcriptional Adaptation of Mycosphaerella graminicola to Programmed Cell Death (PCD) of Its Susceptible Wheat Host". Molecular Plant-Microbe Interactions® 20, n. 2 (febbraio 2007): 178–93. http://dx.doi.org/10.1094/mpmi-20-2-0178.

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Many important fungal pathogens of plants spend long periods (days to weeks) of their infection cycle in symptomless association with living host tissue, followed by a sudden transition to necrotrophic feeding as host tissue death occurs. Little is known about either the host responses associated with this sudden transition or the specific adaptations made by the pathogen to invoke or tolerate it. We are studying a major host-specific fungal pathogen of cultivated wheat, Septoria tritici (teleomorph Mycosphaerella graminicola). Here, we describe the host responses of wheat leaves infected with M. graminicola during the development of disease symptoms and use microarray transcription profiling to identify adaptive responses of the fungus to its changing environment. We show that symptom development on a susceptible host genotype has features reminiscent of the hypersensitive response, a rapid and strictly localized form of host programmed cell death (PCD) more commonly associated with disease-resistance mechanisms. The initiation and advancement of this host response is associated with a loss of cell-membrane integrity and dramatic increases in apoplastic metabolites and the rate of fungal growth. Micro-array analysis of the fungal genes differentially expressed before and after the onset of host PCD supports a transition to more rapid growth. Specific physiological adaptation of the fungus is also revealed with respect to membrane transport, chemical and oxidative stress mechanisms, and metabolism. Our data support the hypothesis that host plant PCD plays an important role in susceptibility towards fungal pathogens with necrotrophic lifestyles.

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Ginger, Michael, e Mark C. Field. "Making the pathogen: Evolution and adaptation in parasitic protists". Molecular and Biochemical Parasitology 209, n. 1-2 (settembre 2016): 1–2. http://dx.doi.org/10.1016/j.molbiopara.2016.11.002.

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Zhabokritsky, Alice, Meherzad Kutky, Lydia A. Burns, Rajita A. Karran e Katalin A. Hudak. "RNA toxins: mediators of stress adaptation and pathogen defense". Wiley Interdisciplinary Reviews: RNA 2, n. 6 (1 agosto 2011): 890–903. http://dx.doi.org/10.1002/wrna.99.

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Bauer, Michael, Sebastian Weis, Mihai G. Netea e Reinhard Wetzker. "Remembering Pathogen Dose: Long-Term Adaptation in Innate Immunity". Trends in Immunology 39, n. 6 (giugno 2018): 438–45. http://dx.doi.org/10.1016/j.it.2018.04.001.

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Fones, H. N., H. McCurrach, A. Mithani, J. A. C. Smith e G. M. Preston. "Local adaptation is associated with zinc tolerance in Pseudomonas endophytes of the metal-hyperaccumulator plant Noccaea caerulescens". Proceedings of the Royal Society B: Biological Sciences 283, n. 1830 (11 maggio 2016): 20160648. http://dx.doi.org/10.1098/rspb.2016.0648.

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Metal-hyperaccumulating plants, which are hypothesized to use metals for defence against pests and pathogens, provide a unique context in which to study plant–pathogen coevolution. Previously, we demonstrated that the high concentrations of zinc found in leaves of the hyperaccumulator Noccaea caerulescens provide protection against bacterial pathogens, with a potential trade-off between metal-based and pathogen-induced defences. We speculated that an evolutionary arms race between zinc-based defences in N. caerulescens and zinc tolerance in pathogens might have driven the development of the hyperaccumulation phenotype. Here, we investigate the possibility of local adaptation by bacteria to the zinc-rich environment of N. caerulescens leaves and show that leaves sampled from the contaminated surroundings of a former mine site harboured endophytes with greater zinc tolerance than those within plants of an artificially created hyperaccumulating population. Experimental manipulation of zinc concentrations in plants of this artificial population influenced the zinc tolerance of recovered endophytes. In laboratory experiments, only endophytic bacteria isolated from plants of the natural population were able to grow to high population densities in any N. caerulescens plants. These findings suggest that long-term coexistence with zinc-hyperaccumulating plants leads to local adaptation by endophytic bacteria to the environment within their leaves.

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Dutta, Anik, Bruce A. McDonald e Daniel Croll. "Combined reference-free and multi-reference based GWAS uncover cryptic variation underlying rapid adaptation in a fungal plant pathogen". PLOS Pathogens 19, n. 11 (16 novembre 2023): e1011801. http://dx.doi.org/10.1371/journal.ppat.1011801.

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Microbial pathogens often harbor substantial functional diversity driven by structural genetic variation. Rapid adaptation from such standing variation threatens global food security and human health. Genome-wide association studies (GWAS) provide a powerful approach to identify genetic variants underlying recent pathogen adaptation. However, the reliance on single reference genomes and single nucleotide polymorphisms (SNPs) obscures the true extent of adaptive genetic variation. Here, we show quantitatively how a combination of multiple reference genomes and reference-free approaches captures substantially more relevant genetic variation compared to single reference mapping. We performed reference-genome based association mapping across 19 reference-quality genomes covering the diversity of the species. We contrasted the results with a reference-free (i.e., k-mer) approach using raw whole-genome sequencing data in a panel of 145 strains collected across the global distribution range of the fungal wheat pathogen Zymoseptoria tritici. We mapped the genetic architecture of 49 life history traits including virulence, reproduction and growth in multiple stressful environments. The inclusion of additional reference genome SNP datasets provides a nearly linear increase in additional loci mapped through GWAS. Variants detected through the k-mer approach explained a higher proportion of phenotypic variation than a reference genome-based approach and revealed functionally confirmed loci that classic GWAS approaches failed to map. The power of GWAS in microbial pathogens can be significantly enhanced by comprehensively capturing structural genetic variation. Our approach is generalizable to a large number of species and will uncover novel mechanisms driving rapid adaptation of pathogens.

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Kupfer, Tom R., e Daniel M. T. Fessler. "Ectoparasite defence in humans: relationships to pathogen avoidance and clinical implications". Philosophical Transactions of the Royal Society B: Biological Sciences 373, n. 1751 (4 giugno 2018): 20170207. http://dx.doi.org/10.1098/rstb.2017.0207.

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Currently, disgust is regarded as the main adaptation for defence against pathogens and parasites in humans. Disgust's motivational and behavioural features, including withdrawal, nausea, appetite suppression and the urge to vomit, defend effectively against ingesting or touching sources of pathogens. However, ectoparasites do not attack their hosts via ingestion, but rather actively attach themselves to the body surface. Accordingly, by itself, disgust offers limited defence against ectoparasites. We propose that, like non-human animals, humans have a distinct ectoparasite defence system that includes cutaneous sensory mechanisms, itch-generation mechanisms and grooming behaviours. The existence of adaptations for ectoparasite defence is supported by abundant evidence from non-human animals, as well as more recent evidence concerning human responses to ectoparasite cues. Several clinical disorders may be dysfunctions of the ectoparasite defence system, including some that are pathologies of grooming, such as skin picking and trichotillomania, and others, such as delusory parasitosis and trypophobia, which are pathologies of ectoparasite detection. We conclude that future research should explore both distinctions between, and overlap across, ectoparasite defence systems and pathogen avoidance systems, as doing so will not only illuminate proximate motivational systems, including disgust, but may also reveal important clinical and social consequences. This article is part of the Theo Murphy meeting issue ‘Evolution of pathogen and parasite avoidance behaviours'.

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TINSLEY, M. C., S. BLANFORD e F. M. JIGGINS. "Genetic variation in Drosophila melanogaster pathogen susceptibility". Parasitology 132, n. 6 (24 febbraio 2006): 767–73. http://dx.doi.org/10.1017/s0031182006009929.

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Genetic variation in susceptibility to pathogens is a central concern both to evolutionary and medical biologists, and for the implementation of biological control programmes. We have investigated the extent of such variation in Drosophila melanogaster, a major model organism for immunological research. We found that within populations, different Drosophila genotypes show wide-ranging variation in their ability to survive infection with the entomopathogenic fungus Beauveria bassiana. Furthermore, striking divergence in susceptibility has occurred between genotypes from temperate and tropical African locations. We hypothesize that this may have been driven by adaptation to local differences in pathogen exposure or host ecology. Genetic variation within populations may be maintained by temporal or spatial variation in the costs and benefits of pathogen defence. Insect pathogens are employed widely as biological control agents and entomopathogenic fungi are currently being developed for reducing malaria transmission by mosquitoes. Our data highlight the need for concern about resistance evolution to these novel biopesticides in vector populations.

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Geoghegan, Jemma L., Alistair M. Senior e Edward C. Holmes. "Pathogen population bottlenecks and adaptive landscapes: overcoming the barriers to disease emergence". Proceedings of the Royal Society B: Biological Sciences 283, n. 1837 (31 agosto 2016): 20160727. http://dx.doi.org/10.1098/rspb.2016.0727.

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Emerging diseases are a major challenge to public health. Revealing the evolutionary processes that allow novel pathogens to adapt to new hosts, also the potential barriers to host adaptation, is central to understanding the drivers of disease emergence. In particular, it is unclear how the genetics and ecology of pathogens interact to shape the likelihood of successful cross-species transmission. To better understand the determinants of host adaptation and emergence, we modelled key aspects of pathogen evolutionary dynamics at both intra- and inter-host scales, using parameter values similar to those observed in influenza virus. We considered the possibility of acquiring the necessary host adaptive mutations both before (‘off-the-shelf’ emergence) and after (‘tailor-made’ emergence) a virus is transmitted from a donor to a new recipient species. Under both scenarios, population bottlenecks at inter-host transmission act as a major barrier to host adaptation, greatly limiting the number of adaptive mutations that are able to cross the species barrier. In addition, virus emergence is hindered if the fitness valley between the donor and recipient hosts is either too steep or too shallow. Overall, our results reveal where in evolutionary parameter space a virus could adapt to and become transmissible in a new species.

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Wendling, Carolin C., e K. Mathias Wegner. "Adaptation to enemy shifts: rapid resistance evolution to local Vibrio spp. in invasive Pacific oysters". Proceedings of the Royal Society B: Biological Sciences 282, n. 1804 (7 aprile 2015): 20142244. http://dx.doi.org/10.1098/rspb.2014.2244.

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One hypothesis for the success of invasive species is reduced pathogen burden, resulting from a release from infections or high immunological fitness of invaders. Despite strong selection exerted on the host, the evolutionary response of invaders to newly acquired pathogens has rarely been considered. The two independent and genetically distinct invasions of the Pacific oyster Crassostrea gigas into the North Sea represent an ideal model system to study fast evolutionary responses of invasive populations. By exposing both invasion sources to ubiquitous and phylogenetically diverse pathogens ( Vibrio spp.), we demonstrate that within a few generations hosts adapted to newly encountered pathogen communities. However, local adaptation only became apparent in selective environments, i.e. at elevated temperatures reflecting patterns of disease outbreaks in natural populations. Resistance against sympatric and allopatric Vibrio spp. strains was dominantly inherited in crosses between both invasion sources, resulting in an overall higher resistance of admixed individuals than pure lines. Therefore, we suggest that a simple genetic resistance mechanism of the host is matched to a common virulence mechanism shared by local Vibrio strains. This combination might have facilitated a fast evolutionary response that can explain another dimension of why invasive species can be so successful in newly invaded ranges.

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Dhillon, Braham, Nicolas Feau, Andrea L. Aerts, Stéphanie Beauseigle, Louis Bernier, Alex Copeland, Adam Foster et al. "Horizontal gene transfer and gene dosage drives adaptation to wood colonization in a tree pathogen". Proceedings of the National Academy of Sciences 112, n. 11 (2 marzo 2015): 3451–56. http://dx.doi.org/10.1073/pnas.1424293112.

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Some of the most damaging tree pathogens can attack woody stems, causing lesions (cankers) that may be lethal. To identify the genomic determinants of wood colonization leading to canker formation, we sequenced the genomes of the poplar canker pathogen,Mycosphaerella populorum, and the closely related poplar leaf pathogen,M. populicola. A secondary metabolite cluster unique toM. populorumis fully activated following induction by poplar wood and leaves. In addition, genes encoding hemicellulose-degrading enzymes, peptidases, and metabolite transporters were more abundant and were up-regulated inM. populorumgrowing on poplar wood-chip medium compared withM. populicola. The secondary gene cluster and several of the carbohydrate degradation genes have the signature of horizontal transfer from ascomycete fungi associated with wood decay and from prokaryotes. Acquisition and maintenance of the gene battery necessary for growth in woody tissues and gene dosage resulting in gene expression reconfiguration appear to be responsible for the adaptation ofM. populorumto infect, colonize, and cause mortality on poplar woody stems.

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Liu, Wei, Shu-Hui Yu, Hong-Ping Zhang, Zuo-Yi Fu, Jia-Qi An, Jin-Yang Zhang e Pu Yang. "Two Cladosporium Fungi with Opposite Functions to the Chinese White Wax Scale Insect Have Different Genome Characters". Journal of Fungi 8, n. 3 (11 marzo 2022): 286. http://dx.doi.org/10.3390/jof8030286.

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Insects encounter infection of microorganisms, and they also harbor endosymbiosis to participate in nutrition providing and act as a defender against pathogens. We previously found the Chinese white wax scale insect, Ericerus pela, was infected and killed by Cladosporium sp. (pathogen). We also found it harbored Cladosporium sp. (endogensis). In this study, we cultured these two Cladosporium fungi and sequenced their genome. The results showed Cladosporium sp. (endogensis) has a larger genome size and more genes than Cladosporium sp. (pathogen). Pan-genome analysis showed Cladosporium sp. (endogensis)-specific genes enriched in pathways related to nutrition production, such as amino acid metabolism, carbohydrate metabolism, and energy metabolism. These pathways were absent in that of Cladosporium sp. (pathogen). Gene Ontology analysis showed Cladosporium sp. (pathogen)-specific genes enriched in the biosynthesis of asperfuranone, emericellamide, and fumagillin. These terms were not found in that of Cladosporium sp. (endogensis). Pathogen Host Interactions analysis found Cladosporium sp. (endogensis) had more genes related to loss of pathogenicity and reduced virulence than Cladosporium sp. (pathogen). Cytotoxicity assay indicated Cladosporium sp. (pathogen) had cytotoxicity, while Cladosporium sp. (endogensis) had no cytotoxicity. These characters reflect the adaptation of endosymbiosis to host-restricted lifestyle and the invader of the entomopathogen to the host.

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Gutiérrez, Saray, Julia Fischer, Raja Ganesan, Nina Judith Hos, Gökhan Cildir, Martina Wolke, Alberto Pessia et al. "Salmonella Typhimurium impairs glycolysis-mediated acidification of phagosomes to evade macrophage defense". PLOS Pathogens 17, n. 9 (23 settembre 2021): e1009943. http://dx.doi.org/10.1371/journal.ppat.1009943.

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Regulation of cellular metabolism is now recognized as a crucial mechanism for the activation of innate and adaptive immune cells upon diverse extracellular stimuli. Macrophages, for instance, increase glycolysis upon stimulation with pathogen-associated molecular patterns (PAMPs). Conceivably, pathogens also counteract these metabolic changes for their own survival in the host. Despite this dynamic interplay in host-pathogen interactions, the role of immunometabolism in the context of intracellular bacterial infections is still unclear. Here, employing unbiased metabolomic and transcriptomic approaches, we investigated the role of metabolic adaptations of macrophages upon Salmonella enterica serovar Typhimurium (S. Typhimurium) infections. Importantly, our results suggest that S. Typhimurium abrogates glycolysis and its modulators such as insulin-signaling to impair macrophage defense. Mechanistically, glycolysis facilitates glycolytic enzyme aldolase A mediated v-ATPase assembly and the acidification of phagosomes which is critical for lysosomal degradation. Thus, impairment in the glycolytic machinery eventually leads to decreased bacterial clearance and antigen presentation in murine macrophages (BMDM). Collectively, our results highlight a vital molecular link between metabolic adaptation and phagosome maturation in macrophages, which is targeted by S. Typhimurium to evade cell-autonomous defense.

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Taliadoros, Demetris, Alice Feurtey, Nathan Wyatt, Benoit Barrès, Pierre Gladieux, Timothy Friesen e Eva H. Stukenbrock. "Emergence and spread of the barley net blotch pathogen coincided with crop domestication and cultivation history". PLOS Genetics 20, n. 1 (29 gennaio 2024): e1010884. http://dx.doi.org/10.1371/journal.pgen.1010884.

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Fungal pathogens cause devastating disease in crops. Understanding the evolutionary origin of pathogens is essential to the prediction of future disease emergence and the potential of pathogens to disperse. The fungus Pyrenophora teres f. teres causes net form net blotch (NFNB), an economically significant disease of barley. In this study, we have used 104 P. teres f. teres genomes from four continents to explore the population structure and demographic history of the fungal pathogen. We showed that P. teres f. teres is structured into populations that tend to be geographically restricted to different regions. Using Multiple Sequentially Markovian Coalescent and machine learning approaches we demonstrated that the demographic history of the pathogen correlates with the history of barley, highlighting the importance of human migration and trade in spreading the pathogen. Exploring signatures of natural selection, we identified several population-specific selective sweeps that colocalized with genomic regions enriched in putative virulence genes, and loci previously identified as determinants of virulence specificities by quantitative trait locus analyses. This reflects rapid adaptation to local hosts and environmental conditions of P. teres f. teres as it spread with barley. Our research highlights how human activities can contribute to the spread of pathogens that significantly impact the productivity of field crops.

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Levy, Hila, Steven R. Fiddaman, Juliana A. Vianna, Daly Noll, Gemma V. Clucas, Jasmine K. H. Sidhu, Michael J. Polito et al. "Evidence of Pathogen-Induced Immunogenetic Selection across the Large Geographic Range of a Wild Seabird". Molecular Biology and Evolution 37, n. 6 (25 febbraio 2020): 1708–26. http://dx.doi.org/10.1093/molbev/msaa040.

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Abstract Over evolutionary time, pathogen challenge shapes the immune phenotype of the host to better respond to an incipient threat. The extent and direction of this selection pressure depend on the local pathogen composition, which is in turn determined by biotic and abiotic features of the environment. However, little is known about adaptation to local pathogen threats in wild animals. The Gentoo penguin (Pygoscelis papua) is a species complex that lends itself to the study of immune adaptation because of its circumpolar distribution over a large latitudinal range, with little or no admixture between different clades. In this study, we examine the diversity in a key family of innate immune genes—the Toll-like receptors (TLRs)—across the range of the Gentoo penguin. The three TLRs that we investigated present varying levels of diversity, with TLR4 and TLR5 greatly exceeding the diversity of TLR7. We present evidence of positive selection in TLR4 and TLR5, which points to pathogen-driven adaptation to the local pathogen milieu. Finally, we demonstrate that two positively selected cosegregating sites in TLR5 are sufficient to alter the responsiveness of the receptor to its bacterial ligand, flagellin. Taken together, these results suggest that Gentoo penguins have experienced distinct pathogen-driven selection pressures in different environments, which may be important given the role of the Gentoo penguin as a sentinel species in some of the world’s most rapidly changing environments.

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LAINE, A. L. "Spatial scale of local adaptation in a plant-pathogen metapopulation". Journal of Evolutionary Biology 18, n. 4 (luglio 2005): 930–38. http://dx.doi.org/10.1111/j.1420-9101.2005.00933.x.

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Ultee, Annemieke, Edwin P. W. Kets, Mark Alberda, Folkert A. Hoekstra e Eddy J. Smid. "Adaptation of the food-borne pathogen Bacillus cereus to carvacrol". Archives of Microbiology 174, n. 4 (25 settembre 2000): 233–38. http://dx.doi.org/10.1007/s002030000199.

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Bernier, Steve P., Matthew L. Workentine e Michael G. Surette. "Genetic signature of bacterial pathogen adaptation during chronic pulmonary infections". Nature Genetics 46, n. 1 (27 dicembre 2013): 5–6. http://dx.doi.org/10.1038/ng.2859.

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Siddle, Katherine J., e Lluis Quintana-Murci. "The Red Queen's long race: human adaptation to pathogen pressure". Current Opinion in Genetics & Development 29 (dicembre 2014): 31–38. http://dx.doi.org/10.1016/j.gde.2014.07.004.

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Nair, Tripti, Brandy Weathers, Nicole Stuhr, James Nhan, Vandita Gorla e Sean Curran. "PATHOGEN APATHY RESULTING FROM SKN-1 ACTIVATION: A MARK OF RESILIENCE OR A RATTLED GUT FEELING?" Innovation in Aging 7, Supplement_1 (1 dicembre 2023): 1094. http://dx.doi.org/10.1093/geroni/igad104.3514.

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Abstract Innate immunity is a key driver in promoting survival against xenobiotic stressors and hostile environments and an appropriate immune response is essential to organismal health across lifespan. Caenorhabditis elegans encounter pathogens in their natural environment and initiate cytoprotective and immune responses that can have long-lasting effects on health, even after the pathogen has been neutralized. Pseudomonas aeruginosa (PA14) is an opportunistic pathogen that is lethal to C. elegans with prolonged exposure. C. elegans employ multiple defense mechanisms to ensure survival upon exposure to pathogens to defend against the current infection and to avoid continued exposure, including activation of the key cytoprotective transcription factor SKN-1 (mammalian homologue Nrf2). Although wild type C. elegans quickly learn to avoid pathogens, our current work documents a peculiar apathy to pathogen in animals with constitutive activation of SKN-1. The outcome is surprising as the role of SKN-1 is to protect an animal from intracellular and environmental insults. This behavior is mediated by tissue specific actions of SKN-1 that initiate cell non-autonomous responses for pathogen avoidance, survival, and metabolic adaptation. Based on transcriptional signature of animals with SKN-1 activation upon exposure to PA14 we observed that the apathy behavior is independent of somatic lipid depletion, thus uncoupling these two exceptional physiological responses. Further, we define the role of neurosignalling molecules in the gut-brain axis that drive the apathy response to pathogens. Our work reveals new insights into how animals perceive pathogens in the environment and subsequently alter behavior and cellular programs to promote survival.

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Mourkas, Evangelos, Aidan J. Taylor, Guillaume Méric, Sion C. Bayliss, Ben Pascoe, Leonardos Mageiros, Jessica K. Calland et al. "Agricultural intensification and the evolution of host specialism in the enteric pathogen Campylobacter jejuni". Proceedings of the National Academy of Sciences 117, n. 20 (4 maggio 2020): 11018–28. http://dx.doi.org/10.1073/pnas.1917168117.

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Modern agriculture has dramatically changed the distribution of animal species on Earth. Changes to host ecology have a major impact on the microbiota, potentially increasing the risk of zoonotic pathogens being transmitted to humans, but the impact of intensive livestock production on host-associated bacteria has rarely been studied. Here, we use large isolate collections and comparative genomics techniques, linked to phenotype studies, to understand the timescale and genomic adaptations associated with the proliferation of the most common food-born bacterial pathogen (Campylobacter jejuni) in the most prolific agricultural mammal (cattle). Our findings reveal the emergence of cattle specialist C. jejuni lineages from a background of host generalist strains that coincided with the dramatic rise in cattle numbers in the 20th century. Cattle adaptation was associated with horizontal gene transfer and significant gene gain and loss. This may be related to differences in host diet, anatomy, and physiology, leading to the proliferation of globally disseminated cattle specialists of major public health importance. This work highlights how genomic plasticity can allow important zoonotic pathogens to exploit altered niches in the face of anthropogenic change and provides information for mitigating some of the risks posed by modern agricultural systems.

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