Academic literature on the topic 'Necrotroph'
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Journal articles on the topic "Necrotroph"
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Shi, Gongjun, Zengcui Zhang, Timothy L. Friesen, Dina Raats, Tzion Fahima, Robert S. Brueggeman, Shunwen Lu, et al. "The hijacking of a receptor kinase–driven pathway by a wheat fungal pathogen leads to disease." Science Advances 2, no. 10 (October 2016): e1600822. http://dx.doi.org/10.1126/sciadv.1600822.
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Necrotrophic pathogens live and feed on dying tissue, but their interactions with plants are not well understood compared to biotrophic pathogens. The wheatSnn1gene confers susceptibility to strains of the necrotrophic pathogenParastagonospora nodorumthat produce the SnTox1 protein. We report the positional cloning ofSnn1, a member of the wall-associated kinase class of receptors, which are known to drive pathways for biotrophic pathogen resistance. Recognition of SnTox1 bySnn1activates programmed cell death, which allows this necrotroph to gain nutrients and sporulate. These results demonstrate that necrotrophic pathogens such asP. nodorumhijack host molecular pathways that are typically involved in resistance to biotrophic pathogens, revealing the complex nature of susceptibility and resistance in necrotrophic and biotrophic pathogen interactions with plants.
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McGrann, Graham R. D., Steven Miller, and Neil D. Havis. "The ENHANCED MAGNAPORTHE RESISTANCE 1 locus affects Ramularia leaf spot development in barley." European Journal of Plant Pathology 156, no. 1 (November 14, 2019): 123–32. http://dx.doi.org/10.1007/s10658-019-01869-x.
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AbstractRamularia leaf spot (RLS) is a newly-important disease of barley which is caused when the fungus Ramularia collo-cygni enters necrotrophic development during colonisation of the host. Mutant alleles at the barley MILDEW LOCUS O, mlo, locus confer broad spectrum durable resistance against the powdery mildew fungus, Blumeria graminis f. sp. hordei, but can enhance susceptibility to pathogens with necrotrophic development stages such as R. collo-cygni. Given the importance of mlo in spring barley breeding programmes, identifying loci that mitigate the effect of mlo-mediated susceptibility on necrotrophic disease development is an important target. Mutation of the ENHANCED MAGNAPORTHE 1 (emr1) locus which can affect mlo-associated disease susceptibility, leads to a reduction in RLS symptoms on barley leaves but does not reduce R. collo-cygni accumulation. The effect of emr1 on the transition of R. collo-cygni from endophyte to necrotroph may relate to changes in reactive oxygen species in mutant plants which show reduced sensitivity to chloroplastic superoxide induced cell death and has lower relative chlorophyll content compared to mlo plants.
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Laluk, Kristin, and Tesfaye Mengiste. "Necrotroph Attacks on Plants: Wanton Destruction or Covert Extortion?" Arabidopsis Book 8 (January 2010): e0136. http://dx.doi.org/10.1199/tab.0136.
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Liang, Xiaofei, and Jeffrey A. Rollins. "Mechanisms of Broad Host Range Necrotrophic Pathogenesis in Sclerotinia sclerotiorum." Phytopathology® 108, no. 10 (October 2018): 1128–40. http://dx.doi.org/10.1094/phyto-06-18-0197-rvw.
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Among necrotrophic fungi, Sclerotinia sclerotiorum is remarkable for its extremely broad host range and for its aggressive host tissue colonization. With full genome sequencing, transcriptomic analyses and the increasing pace of functional gene characterization, the factors underlying the basis of this broad host range necrotrophic pathogenesis are now being elucidated at a greater pace. Among these, genes have been characterized that are required for infection via compound appressoria in addition to genes associated with colonization that regulate oxalic acid (OA) production and OA catabolism. Moreover, virulence-related secretory proteins have been identified, among which are candidates for manipulating host activities apoplastically and cytoplasmically. Coupled with these mechanistic studies, cytological observations of the colonization process have blurred the heretofore clear-cut biotroph versus necrotroph boundary. In this review, we reexamine the cytology of S. sclerotiorum infection and put more recent molecular and genomic data into the context of this cytology. We propose a two-phase infection model in which the pathogen first evades, counteracts and subverts host basal defense reactions prior to killing and degrading host cells. Spatially, the pathogen may achieve this via the production of compatibility factors/effectors in compound appressoria, bulbous subcuticular hyphae, and primary invasive hyphae. By examining the nuances of this interaction, we hope to illuminate new classes of factors as targets to improve our understanding of broad host range necrotrophic pathogens and provide the basis for understanding corresponding host resistance.
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Craven, Kelly D., Heriberto Vélëz, Yangrae Cho, Christopher B. Lawrence, and Thomas K. Mitchell. "Anastomosis Is Required for Virulence of the Fungal Necrotroph Alternaria brassicicola." Eukaryotic Cell 7, no. 4 (February 29, 2008): 675–83. http://dx.doi.org/10.1128/ec.00423-07.
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ABSTRACTA fungal mycelium is typically composed of radially extending hyphal filaments interconnected by bridges created through anastomoses. These bridges facilitate the dissemination of nutrients, water, and signaling molecules throughout the colony. In this study, we used targeted gene deletion and nitrate utilization mutants of the cruciferous pathogenAlternaria brassicicolaand two closely related species to investigate hyphal fusion (anastomosis) and its role in the ability of fungi to cause disease. All eight of theA. brassicicolaisolates tested, as well asA. mimiculaandA. japonica, were capable of self-fusion, with two isolates ofA. brassicicolabeing capable of non-self-fusion. Disruption of the anastomosis gene homolog (Aso1) inA. brassicicolaresulted in both the loss of self-anastomosis and pathogenicity on cabbage. This finding, combined with our discovery that a previously described nonpathogenicA. brassicicolamutant defective for a mitogen-activated protein kinase gene (amk1) also lacked the capacity for self-anastomosis, suggests that self-anastomosis is associated with pathogenicity inA. brassicicola.
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Derbyshire, Mark C., and Sylvain Raffaele. "Till death do us pair: Co-evolution of plant–necrotroph interactions." Current Opinion in Plant Biology 76 (December 2023): 102457. http://dx.doi.org/10.1016/j.pbi.2023.102457.
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Sierota, Zbigniew, and Wojciech Grodzki. "Picea abies–Armillaria–Ips: A Strategy or Coincidence?" Forests 11, no. 9 (September 22, 2020): 1023. http://dx.doi.org/10.3390/f11091023.
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Norway spruce trees weakened by soil drought and progressive die-off of mycorrhizas in root systems become susceptible to infection by rhizomorphs of Armillaria spp. The developing mycelium of this necrotroph induces resin channels in wood, and the induced resin releases some volatile compounds which falsely signal bark beetles that it is safe to invade the host. As a result of the developing beetle outbreak, host trees die, becoming a long-term stock of substrate for the fungus in its saprotrophic stage. This hypothesis is discussed as a fungal survival strategy.
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Ederli, Luisa, Gianandrea Salerno, and Mara Quaglia. "In the tripartite combination Botrytis cinerea–Arabidopsis–Eurydema oleracea, the fungal pathogen alters the plant–insect interaction via jasmonic acid signalling activation and inducible plant-emitted volatiles." Journal of Plant Research 134, no. 3 (March 18, 2021): 523–33. http://dx.doi.org/10.1007/s10265-021-01273-9.
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AbstractIn ecosystems, plants are continuously challenged by combined stress conditions more than by a single biotic or abiotic factor. Consequently, in recent years studies on plant relationships with multiple stresses have aroused increasing interest. Here, the impact of inoculation with fungal pathogens with different lifestyles on Arabidopsis plants response to the following infestation with the invasive crop pest Eurydema oleracea was investigated. In particular, as fungal pathogens the necrotroph Botrytis cinerea and the biotroph Golovinomyces orontii were used. Plants exposed to B. cinerea, but not to G. orontii, showed reduced herbivore feeding damage. This difference was associated to different hormonal pathways triggered by the pathogens: G. orontii only induced the salicylate-mediated pathway, while B. cinerea stimulated also the jasmonate-dependent signalling, which persisted for a long time providing a long-term defence to further herbivore attack. In particular, the lower susceptibility of B. cinerea-infected Arabidopsis plants to E. oleracea was related to the stimulation of the JA-induced pathway on the production of plant volatile compounds, since treatment with VOCs emitted by B. cinerea inoculated plants inhibited both insect plant choice and feeding damage. These results indicate that necrotrophic plant pathogenic fungi modulate host volatile emission, thus affecting plant response to subsequent insect, thereby increasing the knowledge on tripartite plant–microbe–insect interactions in nature.
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Kumari, Anita, Abhijeet Ghatak, and Srinivasaraghavan A. "Biochemical responses of soil-borne necrotroph Sclerotium rolfsii during the pathogenesis on chickpea." International Journal of Chemical Studies 8, no. 1 (January 1, 2020): 2596–601. http://dx.doi.org/10.22271/chemi.2020.v8.i1an.8661.
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Bailey, Bryan A., Shahin S. Ali, Mary D. Strem, and Lyndel W. Meinhardt. "Morphological variants of Moniliophthora roreri on artificial media and the biotroph/necrotroph shift." Fungal Biology 122, no. 7 (July 2018): 701–16. http://dx.doi.org/10.1016/j.funbio.2018.03.003.
Full textDissertations / Theses on the topic "Necrotroph"
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com, rohanlowe@gmail, and Rohan George Thomas Lowe. "Sporulation of Stagonospra nodorum." Murdoch University, 2006. http://wwwlib.murdoch.edu.au/adt/browse/view/adt-MU20071101.221432.
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Stagonospora nodorum is a necrotrophic fungal pathogen that is the causal agent of leaf and glume blotch on wheat. Very little is currently known about the molecular mechanisms required for pathogenicity of S. nodorum, despite its major impact on Australian agriculture. S. nodorum is a polycyclic pathogen. Rain-splashed pycnidiospores attach to and colonise wheat tissue and subsequently sporulate within 2-3 weeks. Several cycles of infection are needed to build up inoculum for the damaging infection of flag leaves and heads, sporulation is therefore a critical component of the infection cycle of S. nodorum; our aim is to determine the genetic and biochemical requirements for sporulation for development of control of the pathogen. Disease progression of S. nodorum on wheat cv. Amery was monitored by light microscopy to determine the time point when pycnidia development began. Early pycnidia development was evident 12 days post-infection. This information was used to guide a genomics and a metabolomics based approach to determine the requirements for sporulation in S. nodorum. The genomics approach utilised two cDNA libraries created from sporulating and non-sporulating cultures. EST frequency was used to determine highly expressed genes under the two developmental states. Gene expression from the most highly represented genes during sporulation were confirmed using quantitative PCR. A gene encoding an arabitol 4-dehydrogenase (Abd1), was mutagenised, in its absence sporulation was reduced by approximately 20%. The metabolomics approach isolated metabolites from both in planta infection and in vitro growth. Rapid changes in the abundance of metabolites were detected during the onset of sporulation. Key fungal metabolites identified include mannitol and trehalose. The concentration of both mannitol and trehalose increased dramatically in concert with pycnidia formation. Both mannitol and trehalose have also been linked to pathogenicity in filamentous fungi. Creation of deletion mutants of the gene encoding trehalose 6-phosphate synthase showed the synthesis of trehalose is required for full sporulation of S. nodorum in planta and in vitro.
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Shouan, Liu [Verfasser], Paul [Akademischer Betreuer] Schulze-Lefert, and Ulf-Ingo [Akademischer Betreuer] Flügge. "The role of Arabidopsis WRKY33 in modulating host immunity towards the necrotroph Botrytis cinerea / Liu Shouan. Gutachter: Paul Schulze-Lefert ; Ulf-Ingo Flügge." Köln : Universitäts- und Stadtbibliothek Köln, 2015. http://d-nb.info/1075316944/34.
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Sprockett, Daniel David. "The Evolution of Fungal Pectinases in Glycosyl Hydrolase Family 28 and Their Association with Ecological Strategy." Kent State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=kent1259688919.
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Badet, Thomas. "Genome scale analysis of Arabidopsis thaliana quantitative disease resistance to the generalist fungal pathogen Sclerotinia sclerotiorum." Electronic Thesis or Diss., Toulouse 3, 2017. http://www.theses.fr/2017TOU30403.
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Les interactions entre plantes et agents pathogènes sont fréquentes dans la nature, mais conduisent rarement à une maladie. En effet, les plantes ont un système immunitaire efficace capable de faire face à la plupart des attaques microbiennes. Les agents pathogènes fongiques représentent néanmoins une menace majeure pour la sécurité alimentaire dans le monde. Sclerotinia sclerotiorum est un champignon pathogène de la famille des Ascomycetes responsable de la maladie de la pourriture blanche sur des centaines d'espèce de plantes. Il n'y a aucune source génétique de résistance complète à ce pathogène connue et les moyens de lutte reposent essentiellement sur l'utilisation de fongicides. Mieux comprendre les bases moléculaires de l'interaction entre S. sclerotiorum et ses plantes hôtes est indispensable à l'amélioration des cultures végétales. La résistance à S. sclerotiorum se caractérise par un continuum de symptômes dans les populations végétales naturelles. Cette observation suggère que la résistance est contrôlée par de multiples gènes, un phénotype appelé résistance quantitative (QDR). Mon projet de thèse a consisté dans une première partie à identifier les mécanismes moléculaires sous-jacents à la QDR vis-à-vis de S. sclerotiorum dans des accessions naturelles de la plante modèle Arabidopsis thaliana. Une analyse de génétique d'association à l'échelle du génome (GWA) m'a permis d'associer la variabilité génétique avec le niveau résistance à S. sclerotiorum et d'identifier trois loci potentiellement impliqués dans la QDR à S. sclerotiorum. J'ai effectué l'analyse fonctionnelle des gènes candidats et étudié la diversité génétique à ces différents loci. Mes résultats ont révélé qu'une prolyl-oligopeptidase (POQR) et une protéine reliée au complexe d'actine (ARPC4) sont impliqués dans la résistance quantitative à S. sclerotiorum. L'étude du réseau d'actine par microscopie confocale a révélé le rôle des filaments d'actine dans la réponse immunitaire à S. sclerotiorum. Je montre par ailleurs que l'allèle de POQR conférant résistance à S. sclerotiorum a évolué de façon convergente chez plusieurs espèces de plantes, suggérant que certains mécanismes de la QDR sont communs à différentes espèces végétales. Alors que de nombreux champignons pathogènes ne sont capables d'infecter que quelques génotypes de plantes, S. sclerotiorum est un agent pathogène dit généraliste, c'est-à-dire capable d'infecter de nombreuses espèces d'hôtes. Dans la deuxième partie du projet, je me suis intéressé aux propriétés du génome de S. sclerotiorum associées à son caractère généraliste. La théorie prédit que le généralisme est coûteux énergétiquement, si bien qu'il doit engendrer d'importants compromis avec d'autres traits. Au niveau génétique, certains codons (triplets de nucléotides) permettent une traduction plus efficace que leurs synonymes. En effet, le code génétique décryptant ADN/ARN en protéines est redondant, plusieurs codons pouvant coder pour le même acide aminé. Optimiser l'usage de codons au niveau du génome permet ainsi de réduire les coûts liés à la production de protéines. J'ai analysé l'usage de codons chez les 45 espèces fongiques et révélé que les séquences codantes chez les espèces de pathogènes généralistes étaient fortement optimisées. Par ailleurs, je montre que les codons adaptés sont sous sélection purifiante dans une population naturelle de S. sclerotiorum, suggérant que l'optimisation de l'usage de codons est une adaptation évolutive au généralisme chez les champignons parasitesIn nature, plant pathogen interactions are frequent but disease is not the most prevalent outcome. Indeed, plants evolved an efficient immune system able to face multiple pathogen attacks. Getting insights into plant microbe interactions at multiple levels will improve our understanding of how plants defend against pathogens and help building sustainable agronomy. Fungal plant pathogens are major threats to food security worldwide. Sclerotinia sclerotiorum is an Ascomycete generalist plant pathogen causing mold diseases on hundreds of plant species. There is no genetic source of complete plant resistance to this generalist pathogen known to date. Instead, natural plant populations show a continuum of resistance levels controlled by multiple genes, a phenotype designated as quantitative disease resistance (QDR). Little is known about the molecular mechanisms controlling the interaction between plants and S. sclerotiorum, and more generally which are the molecular bases underlying QDR in plants. My thesis project consisted in a first part in identifying molecular mechanisms underlying QDR to S. sclerotiorum in natural accessions of the model plant Arabidopsis thaliana. A Genome wide association study (GWAS) allowed me to associate genetic variation with disease resistance to S. sclerotiorum. The analysis pinpointed three genes in A. thaliana genome as putative candidates involved in QDR to S. sclerotiorum. I led the functional characterization of these genes and investigated natural diversity at these loci. The results revealed that a prolyl-oligopeptidase (POQR) and an actin-related protein complex member (ARPC4) are associated with QDR against S. sclerotiorum. The analysis of actin filament networks highlighted their role in response to S. sclerotiorum. Furthermore, I showed that POQR alleles evolved convergently in different plant lineages, suggesting that some QDR molecular mechanisms are conserved across plants. Among fungal parasites, some like S. sclerotiorum are able to infect multiple species while others are restricted to one or few hosts. In the second part of the project, I investigated the properties of S. sclerotiorum genome associated to its ability to infect hundreds of plant species. Theory predicts that generalism comes at a cost and may underlie important fitness trade-offs. At the genome level, some codons (nucleotide triplets) allow more efficient translation than their synonymous. Indeed, the genetic encoding of proteins is redundant with multiple codons specifying the same amino acid. The optimization of codon-usage is a mean to reduce the costs associated with protein production. I analysed codon-usage at the genome level in 45 fungal species to reveal that generalist parasites are highly codon optimized. Moreover, I showed that optimized codons are under purifying selection, suggesting that codon optimization is an adaptation to generalist parasitism in fungi
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Kaile, Androulla. "The role of calcium in necrotrophic plant pathogenesis." Thesis, University of Exeter, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.253532.
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Miller, Laurie. "Studies on CBH1 : a cellobiohydrolase of Sclerotinia sclerotiorum." Thesis, University of Sheffield, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364190.
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Gao, Yuanyuan. "Identification and Functional Characterization of Necrotrophic Effectors in Parastagonospora Nodorum." Diss., North Dakota State University, 2015. http://hdl.handle.net/10365/25490.
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The necrotrophic fungus Parastagonospora nodorum (teleomorph; Phaeosphaeria
nodorum), is the causal agent of Septoria nodorum blotch (SNB) on common wheat (Triticum
aestivum L.) and durum wheat (Triticum turgidum L.). SNB is a serious foliar and glume disease
which causes significant yield losses in major wheat growing areas and has serious impact on
grain quality. P. nodorum produces necrotrophic effectors (NEs) that are recognized by and
interact with dominant host sensitivity genes in an inverse gene-for-gene manner. The NE-host
interaction is critical to induce necrotrophic effector-triggered susceptibility (NETS), resulting in
SNB disease. To date, nine NE-host sensitivity gene interactions, following a NETS model, have
been identified in the P. nodorum-wheat pathosystem. One of the NE-host sensitivity gene
interactions, SnTox6-Snn6 interaction was characterized in this study. The SnTox6-Snn6
interaction was shown to be light dependent and Snn6 was located to a major disease
susceptibility QTL on wheat chromosome 6A. SnTox1, another NE first identified in our lab,
interacts with the corresponding wheat sensitivity gene Snn1. SnTox1 was further characterized
in this study. The SnTox1 protein harbors C-terminal domains with a high degree of structural
homology to plant chitin binding proteins and was subsequently shown to bind chitin, a main
component of the fungal cell wall. Therefore, SnTox1 was hypothesized to compete with wheat
chitinases to bind chitin, preventing fungal cell wall degradation. To investigate this hypothesis,
the SnTox1 binding affinity with chitin was tested, as well as its potential function in the
protection against chitinases during fungal mycelial growth. To identify additional NE regions,
genome wide association study (GWAS) technology was used. A global collection of 191 P.
nodorum isolates were genotyped using a restriction-site associated DNA genotyping by
sequencing (RAD-GBS) protocol to identify SNP markers. Phenotypic data including fungal
inoculations and culture filtrate infiltrations were collected using 191 P. nodorum isolates across
several wheat lines. GWAS analyses were performed by regressing the phenotypic data and
genotypic data by running multiple GWAS models.
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Hutchens, Andrew R. "Ambient pH- and carbon-regulated gene expression in the necrotrophic phytopathogen Sclerotinia sclerotiorum." [Gainesville, Fla.] : University of Florida, 2005. http://purl.fcla.edu/fcla/etd/UFE0011843.
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Lundén, Karl. "Heterobasidion - conifer pathosystem : heterologous array analysis and transcriptional shift from saprotrophic to necrotrophic growth /." Uppsala : Department of Forest Mycology and Pathology, Swedish University of Agricultural Sciences, 2010. http://epsilon.slu.se/201019.pdf.
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Hane, James. "Bioinformatic genome analysis of the necrotrophic wheat-pathogenic fungus Phaeosphaeria nodorum and related Dothideomycete fungi." Thesis, Hane, James (2011) Bioinformatic genome analysis of the necrotrophic wheat-pathogenic fungus Phaeosphaeria nodorum and related Dothideomycete fungi. PhD thesis, Murdoch University, 2011. https://researchrepository.murdoch.edu.au/id/eprint/5803/.
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Phaeosphaeria nodorum (anamorph: Stagonospora nodorum) is the causal agent of Stagonospora nodorum blotch (SNB, syn. glume blotch) in wheat. P. nodorum is estimated to cause up to 31% wheat yield loss worldwide. Within Australia it is the primary pathogen of wheat and is estimated to cause losses of $108 million per annum. The genome assembly of P. nodorum was sequenced in 2005 and was the first species in the class Dothideomycetes, a significant fungal taxon containing several major phytopathogens, to be publically released. The P. nodorum genome database has since evolved from basic sequence data into a powerful resource for studying the SNB host-pathogen interaction and advancing the understanding of fungal genome structure. The genes of P. nodorum have been annotated to a high level of accuracy and now serve as a model dataset for comparative purposes. P. nodorum gene annotations have been refined by a combination of several techniques including manual curation, orthology with related species, expressed sequence tag (EST) alignment, and proteogenomics. Analysis of the repetitive DNA in the P. nodorum genome lead to the development of software for the analysis of repeat-induced point mutation (RIP), a fungal-specific genome defence mechanism, which was a major improvement upon previous methods. Comparative genomics between P. nodorum and related species has highlighted a novel pattern of genome sequence conservation between filamentous fungi called ‘mesosynteny’ and has lead to the development of novel 'genome finishing' strategies.
Books on the topic "Necrotroph"
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De Cal, Antonieta, Maria Del Mar Jimenez-Gasco, and Paloma Melgarejo, eds. Necrotrophic Fungal Plant Pathogens. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88974-623-1.
Full textBook chapters on the topic "Necrotroph"
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Hahn, Matthias, Muriel Viaud, and Jan van Kan. "The Genome of Botrytis cinerea, a Ubiquitous Broad Host Range Necrotroph." In Genomics of Plant-Associated Fungi and Oomycetes: Dicot Pathogens, 19–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-662-44056-8_2.
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Geeta and Reema Mishra. "Fungal and Bacterial Biotrophy and Necrotrophy." In Molecular Aspects of Plant-Pathogen Interaction, 21–42. Singapore: Springer Singapore, 2018. http://dx.doi.org/10.1007/978-981-10-7371-7_2.
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Karlsson, Magnus, Lea Atanasova, Dan Funck Jensen, and Susanne Zeilinger. "Necrotrophic Mycoparasites and Their Genomes." In The Fungal Kingdom, 1005–26. Washington, DC, USA: ASM Press, 2017. http://dx.doi.org/10.1128/9781555819583.ch50.
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Ayliffe, Michael, Ming Luo, Justin Faris, and Evans Lagudah. "Disease Resistance." In Wheat Improvement, 341–60. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-030-90673-3_19.
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AbstractWheat plants are infected by diverse pathogens of economic significance. They include biotrophic pathogens like mildews and rusts that require living plant cells to proliferate. By contrast necrotrophic pathogens that cause diseases such as tan spot, Septoria nodurum blotch and spot blotch require dead or dying cells to acquire nutrients. Pioneering studies in the flax plant-flax rust pathosystem led to the ‘gene-for-gene’ hypothesis which posits that a resistance gene product in the host plant recognizes a corresponding pathogen gene product, resulting in disease resistance. In contrast, necrotrophic wheat pathosystems have an ‘inverse gene-for-gene’ system whereby recognition of a necrotrophic fungal product by a dominant host gene product causes disease susceptibility, and the lack of recognition of this pathogen molecule leads to resistance. More than 300 resistance/susceptibility genes have been identified genetically in wheat and of those cloned the majority encode nucleotide binding, leucine rich repeat immune receptors. Other resistance gene types are also present in wheat, in particular adult plant resistance genes. Advances in mutational genomics and the wheat pan-genome are accelerating causative disease resistance/susceptibility gene discovery. This has enabled multiple disease resistance genes to be engineered as a transgenic gene stack for developing more durable disease resistance in wheat.
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Dickman, Marty, Jan van Kan, and Christopher Lawrence. "Necrotrophic Fungi: Live and Let Die." In Cellular and Molecular Biology of Filamentous Fungi, 645–59. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555816636.ch40.
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Horbach, Ralf, and Holger B. Deising. "13 The Biotrophy–Necrotrophy Switch in Fungal Pathogenesis." In Agricultural Applications, 343–60. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-36821-9_13.
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Prell, Hermann H., and Peter Day. "Phytotoxins: The Weapons of Necrotrophic Phytopathogenic Fungi." In Plant-Fungal Pathogen Interaction, 57–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 2001. http://dx.doi.org/10.1007/978-3-662-04412-4_8.
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Rouxel, Thierry, and Pierre J. G. M. de Wit. "Dothideomycete Effectors Facilitating Biotrophic and Necrotrophic Lifestyles." In Effectors in Plant-Microbe Interactions, 195–218. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781119949138.ch8.
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Mathan, L., Namo Dubey, Swati Verma, and Kunal Singh. "Transcription Factors Associated with Defense Response Against Fungal Necrotrophs." In Transcription Factors for Biotic Stress Tolerance in Plants, 61–78. Cham: Springer International Publishing, 2022. http://dx.doi.org/10.1007/978-3-031-12990-2_4.
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Ruiz-Padilla, Ana, Julio L. Rodríguez-Romero, Davide Pacifico, Marco Chiapello, and María A. Ayllón. "Determination of the Mycovirome of a Necrotrophic Fungus." In Methods in Molecular Biology, 83–101. New York, NY: Springer US, 2023. http://dx.doi.org/10.1007/978-1-0716-3515-5_6.
Full textConference papers on the topic "Necrotroph"
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"Functional characterization of Stagonospora nodorum necrotrophic effectors." In Current Challenges in Plant Genetics, Genomics, Bioinformatics, and Biotechnology. Institute of Cytology and Genetics, Siberian Branch of the Russian Academy of Sciences Novosibirsk State University, 2019. http://dx.doi.org/10.18699/icg-plantgen2019-21.
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Kaneps, Janis, Biruta Bankina, and Inga Moročko-Bičevska. "Virulence of Pyrenophora tritici-repentis: a minireview." In Research for Rural Development 2021 : annual 27th International scientific conference proceedings. Latvia University of Life Sciences and Technologies, 2021. http://dx.doi.org/10.22616/rrd.27.2021.003.
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Pyrenophora tritici-repentis is a major wheat pathogen in all wheat (Triticum spp.) growing areas worldwide. Up to date, eight P. tritici-repentis races have been described based on chlorosis, necrosis, or both symptoms caused on race differential wheat genotypes: ‘Glenlea’, 6B662, 6B365, and ‘Salamouni’. Symptom development on differential genotypes depends on the interaction of the pathogen’s necrotrophic effectors named Ptr ToxA, Ptr ToxB, and Ptr ToxC with host susceptibility genes. Ptr ToxA is encoded by the single copy gene ToxA and induces necrosis on sensitive wheat cultivars. Ptr ToxB causes chlorosis and is encoded by the multicopy gene ToxB. The Ptr ToxC is the non-proteinaceous, polar, low molecular mass molecule that also induces chlorosis, but up to date, the gene encoding this toxin is unknown. Races producing Ptr ToxA are predominant in the global Ptr population. There are several reports about new putative races of P. tritici-repentis that do not conform with the current race system, so further research is required. This study aims to collect and systematise available information about the virulence and races of P. tritici-repentis.
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Veselova, Svetlana, Tatyana Nuzhnaya, Guzel Burkhanova, Sergey Rumyantsev, and Igor Maksimov. "Reactive Oxygen Species in Host-Plant Are Required for an Early Defense Response Against Attack of Stagonospora nodorum Berk. Necrotrophic Effectors SnTox." In The 1st International Electronic Conference on Plant Science. Basel, Switzerland: MDPI, 2020. http://dx.doi.org/10.3390/iecps2020-08765.
Full textReports on the topic "Necrotroph"
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Horwitz, Benjamin, and Nicole M. Donofrio. Identifying unique and overlapping roles of reactive oxygen species in rice blast and Southern corn leaf blight. United States Department of Agriculture, January 2017. http://dx.doi.org/10.32747/2017.7604290.bard.
Full textAbstract:
Plants and their fungal pathogens both produce reactive oxygen species (ROS). CytotoxicROS act both as stressors and signals in the plant-fungal interaction. In biotrophs, a compatible interaction generates little ROS, but is followed by disease. An incompatible interaction results in a strong oxidative burst by the host, limiting infection. Necrotrophs, in contrast, thrive on dead and dying cells in an oxidant-rich local environment. Rice blast, Magnaportheoryzae, a hemibiotroph, occurs worldwide on rice and related hosts and can decimate enough rice each year to feed sixty million people. Cochliobolusheterostrophus, a necrotroph, causes Southern corn leaf blight (SLB), responsible for a major epidemic in the 1970s. The objectives of our study of ROS signaling and response in these two cereal pathogens were: Confocal imaging of ROS production using genetically encoded redox sensor in two pathosystems over time. Forward genetic screening of HyPer sensor lines in two pathosystems for fungal genes involved in altered ROSphenotypes. RNA-seq for discovery of genes involved in ROS-related stress and signaling in two pathosystems. Revisions to the research plan: Library construction in SLB was limited by low transformation efficiency, compounded by a protoplasting enzyme being unavailable during most of year 3. Thus Objective 2 for SLB re-focused to construction of sensor lines carrying deletion mutations in known or candidate genes involved in ROS response. Imaging on rice proved extremely challenging, so mutant screening and imaging were done with a barley-infecting line, already from the first year. In this project, ROS imaging at unprecedented time and spatial resolution was achieved, using genetically-encoded ratio sensors in both pathogens. This technology is currently in use for a large library of rice blast mutants in the ROS sensor background, and Southern corn leaf blight mutants in final stages of construction. The imaging methods developed here to follow the redox state of plant pathogens in the host tissue should be applicable to fungal pathogens in general. Upon completion of mutant construction for SCLB we hope to achieve our goal of comparison between intracellular ROS status and response in hemibiotroph and necrotroph cereal pathogens.
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Dickman, Martin B., and Oded Yarden. Modulation of the Redox Climate and Phosphatase Signaling in a Necrotroph: an Axis for Inter- and Intra-cellular Communication that Regulates Development and Pathogenicity. United States Department of Agriculture, August 2011. http://dx.doi.org/10.32747/2011.7697112.bard.
Full textAbstract:
The long-term goals of our research are to understand the regulation of sclerotial development and pathogenicity in S. sclerotiorum. The focus in this project is on the elucidation of the signaling events and environmental cues that contribute to broad pathogenic success of S. sclerotiorum. In this proposal, we have taken advantage of the recent conceptual (ROS/PPs signaling) and technical (genome sequence availability and gene inactivation possibilities) developments to address the following questions, as appear in our research goals stated below, specifically concerning the involvement of REDOX signaling and protein dephosphorylation in the regulation of hyphal/sclerotial development and pathogenicity of S. sclerotiorum. Our stated specific objectives were to progress our understanding of the following questions: (i) Which ROS species affect S. sclerotiorum development and pathogenicity? (ii) In what manner do PPs affect S. sclerotiorum development and pathogenicity? (iii) Are PPs affected by ROS production and does PP activity affect ROS production and SMK1? (iv) How does Sclerotinia modulate the redox environment in both host and pathogen? While addressing these questions, our main findings include the identification and characterization the NADPH oxidase (NOX) family in S. sclerotiorum. Silencing of Ssnox1 indicated a central role for this enzyme in both virulence and pathogenic (sclerotial) development, while inactivation of Ssnox2 resulted in limited sclerotial development but remained fully pathogenic. Interestingly, we found a consistent correlation with Ssnox1(involved with pathogenicity) and oxalate levels. This same observation was also noted with Sssod1. Thus, fungal enzymes involved in oxidative stress tolerance,when inactivated, also exhibit reduced OA levels. We have also shown that protein phosphatases (specifically PP2A and PTP1) are involved in morphogenesis and pathogenesis of S. sclerotiorum, demonstrating the regulatory role of these key proteins in the mentioned processes. While probing the redox environment and host-pathogen interactions we determined that oxalic acid is an elicitor of plant programmed cell death during S. sclerotiorum disease development and that oxalic acid suppresses host defense via manipulation of the host redox environment. During the course of this project we also contributed to the progress of understanding S. sclerotiorum function and the manipulation of this fungus by establishing an efficient gene replacement and direct hyphal transformation protocols in S. sclerotiorum. Lastly, both PIs were involved in thegenomic analysis of this necrotrophic fungal pathogen (along with Botrytis cinerea). Our results have been published in 11 papers (including joint papers and refereed reviews) and have set the basis for a continuum towards a better understanding and eventual control of this important pathogen (with implications to other fungal-host systems as well).
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Dickman, Martin B., and Oded Yarden. Genetic and chemical intervention in ROS signaling pathways affecting development and pathogenicity of Sclerotinia sclerotiorum. United States Department of Agriculture, July 2015. http://dx.doi.org/10.32747/2015.7699866.bard.
Full textAbstract:
Abstract: The long-term goals of our research are to understand the regulation of sclerotial development and pathogenicity in S. sclerotior11111. The focus in this project was on the elucidation of the signaling events and environmental cues involved in the regulation of these processes, utilizing and continuously developing tools our research groups have established and/or adapted for analysis of S. sclerotiorum, Our stated objectives: To take advantage of the recent conceptual (ROS/PPs signaling) and technical (amenability of S. sclerotiorumto manipulations coupled with chemical genomics and next generation sequencing) developments to address and extend our fundamental and potentially applicable knowledge of the following questions concerning the involvement of REDOX signaling and protein dephosphorylation in the regulation of hyphal/sclerotial development and pathogenicity of S. sclerotiorum: (i) How do defects in genes involved in ROS signaling affect S. sclerotiorumdevelopment and pathogenicity? (ii) In what manner do phosphotyrosinephosphatases affect S. sclerotiorumdevelopment and pathogenicity and how are they linked with ROS and other signaling pathways? And (iii) What is the nature of activity of newly identified compounds that affect S. sclerotiori,111 growth? What are the fungal targets and do they interfere with ROS signaling? We have met a significant portion of the specific goals set in our research project. Much of our work has been published. Briefly. we can summarize that: (a) Silencing of SsNox1(NADPHoxidase) expression indicated a central role for this enzyme in both virulence and pathogenic development, while inactivation of the SsNox2 gene resulted in limited sclerotial development, but the organism remained fully pathogenic. (b) A catalase gene (Scatl), whose expression was highly induced during host infection is involved in hyphal growth, branching, sclerotia formation and infection. (c) Protein tyrosine phosphatase l (ptpl) is required for sclerotial development and is involved in fungal infection. (d) Deletion of a superoxidedismutase gene (Sssodl) significantly reduced in virulence on both tomato and tobacco plants yet pathogenicity was mostly restored following supplementation with oxalate. (e) We have participated in comparative genome sequence analysis of S. sclerotiorumand B. cinerea. (f) S. sclerotiorumexhibits a potential switch between biotrophic and necrotrophic lifestyles (g) During plant microbe interactions cell death can occur in both resistant and susceptible events. Non pathogenic fungal mutants S. sclerotior111n also cause a cell death but with opposing results. We investigated PCD in more detail and showed that, although PCD occurs in both circumstances they exhibit distinctly different features. The mutants trigger a restricted cell death phenotype in the host that unexpectedly exhibits markers associated with the plant hypersensitive (resistant) response. Using electron and fluorescence microscopy, chemical effectors and reverse genetics, we have established that this restricted cell death is autophagic. Inhibition of autophagy rescued the non-pathogenic mutant phenotype. These findings indicate that autophagy is a defense response in this interaction Thus the control of cell death, dictated by the plant (autophagy) סr the fungus (apoptosis), is decisive to the outcome of certain plant microbe interactions. In addition to the time and efforts invested towards reaching the specific goals mentioned, both Pls have initiated utilizing (as stated as an objective in our proposal) state of the art RNA-seq tools in order to harness this technology for the study of S. sclerotiorum. The Pls have met twice (in Israel and in the US), in order to discuss .נחd coordinate the research efforts. This included a working visit at the US Pls laboratory for performing RNA-seq experiments and data analysis as well as working on a joint publication (now published). The work we have performed expands our understanding of the fundamental biology (developmental and pathogenic) of S. sclerotioז111וז. Furthermore, based on our results we have now reached the conclusion that this fungus is not a bona fide necrotroph, but can also display a biotrophic lifestyle at the early phases of infection. The data obtained can eventually serve .נ basis of rational intervention with the disease cycle of this pathogen.
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Horwitz, Benjamin A., and Barbara Gillian Turgeon. Fungal Iron Acquisition, Oxidative Stress and Virulence in the Cochliobolus-maize Interaction. United States Department of Agriculture, March 2012. http://dx.doi.org/10.32747/2012.7709885.bard.
Full textAbstract:
Our project focused on genes for high affinity iron acquisition in Cochliobolus heterostrophus, a necrotrophic pathogen of maize, and their intertwined relationship to oxidative stress status and virulence of the fungus on the host. An intriguing question was why mutants lacking the nonribosomal peptide synthetase (NRPS) gene (NPS6) responsible for synthesis of the extracellular siderophore, coprogen, are sensitive to oxidative stress. Our overall objective was to understand the mechanistic connection between iron stress and oxidative stress as related to virulence of a plant pathogen to its host. The first objective was to examine the interface where small molecule peptide and reactive oxygen species (ROS) mechanisms overlap. The second objective was to determine if the molecular explanation for common function is common signal transduction pathways. These pathways, built around sensor kinases, response regulators, and transcription factors may link sequestering of iron, production of antioxidants, resistance to oxidative stress, and virulence. We tested these hypotheses by genetic manipulation of the pathogen, virulence assays on the host plant, and by following the expression of key fungal genes. An addition to the original program, made in the first year, was to develop, for fungi, a genetically encoded indicator of redox state based on the commercially available Gfp-based probe pHyper, designed for animal cell biology. We implemented several tools including a genetically encoded indicator of redox state, a procedure to grow iron-depleted plants, and constructed a number of new mutants in regulatory genes. Lack of the major Fe acquisition pathways results in an almost completely avirulent phenotype, showing how critical Fe acquisition is for the pathogen to cause disease. Mutants in conserved signaling pathways have normal ability to regulate NPS6 in response to Fe levels, as do mutants in Lae1 and Vel1, two master regulators of gene expression. Vel1 mutants are sensitive to oxidative stress, and the reason may be underexpression of a catalase gene. In nps6 mutants, CAT3 is also underexpressed, perhaps explaining the sensitivity to oxidative stress. We constructed a deletion mutant for the Fe sensor-regulator SreA and found that it is required for down regulation of NPS6 under Fe-replete conditions. Lack of SreA, though, did not make the fungus over-sensitive to ROS, though the mutant had a slow growth rate. This suggests that overproduction of siderophore under Fe-replete conditions is not very damaging. On the other hand, increasing Fe levels protected nps6 mutants from inhibition by ROS, implying that Fe-catalyzed Fenton reactions are not the main factor in its sensitivity to ROS. We have made some progress in understanding why siderophore mutants are sensitive to oxidative stress, and in doing so, defined some novel regulatory relationships. Catalase genes, which are not directly related to siderophore biosynthesis, are underexpressed in nps6 mutants, suggesting that the siderophore product (with or without bound Fe) may act as a signal. Siderophores, therefore, could be a target for intervention in the field, either by supplying an incorrect signal or blocking a signal normally provided during infection. We already know that nps6 mutants cause smaller lesions and have difficulty establishing invasive growth in the host. Lae1 and Vel1 are the first factors shown to regulate both super virulence conferred by T-toxin, and basic pathogenicity, due to unknown factors. The mutants are also altered in oxidative stress responses, key to success in the infection court, asexual and sexual development, essential for fungal dissemination in the field, aerial hyphal growth, and pigment biosynthesis, essential for survival in the field. Mutants in genes encoding NADPH oxidase (Nox) are compromised in development and virulence. Indeed the triple mutant, which should lack all Nox activity, was nearly avirulent. Again, gene expression experiments provided us with initial evidence that superoxide produced by the fungus may be most important as a signal. Blocking oxidant production by the pathogen may be a way to protect the plant host, in interactions with necrotrophs such as C. heterostrophus which seem to thrive in an oxidant environment.
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Dickman, Martin B., and Oded Yarden. Characterization of the chorismate mutase effector (SsCm1) from Sclerotinia sclerotiorum. United States Department of Agriculture, January 2015. http://dx.doi.org/10.32747/2015.7600027.bard.
Full textAbstract:
Sclerotinia sclerotiorum is a filamentous fungus (mold) that causes plant disease. It has an extremely wide range of hosts (>400 species) and causes considerable damage (annual multimillion dollar losses) in economically important crops. It has proven difficult to control (culturally or chemically) and host resistance to this fungus has generally been inadequate. It is believed that this fungus occurs in almost every country. Virulence of this aggressive pathogen is bolstered by a wide array of plant cell wall degrading enzymes and various compounds (secondary metabolites) produced by the fungus. It is well established that plant pathogenic fungi secrete proteins and small molecules that interact with host cells and play a critical role in disease development. Such secreted proteins have been collectively designated as “effectors”. Plant resistance against some pathogens can be mediated by recognition of such effectors. Alternatively, effectors can interfere with plant defense. Some such effectors are recognized by the host plant and can culminate in a programmed cell death (PCD) resistant response. During the course of this study, we analyzed an effector in Sclerotiniasclerotiorum. This specific effector, SsCM1 is the protein chorismatemutase, which is an enzyme involved in a pathway which is important in the production of important amino acids, such a Tryptophan. We have characterized the Sclerotiniaeffector, SsCM1, and have shown that inactivation of Sscm1 does not affect fungal vegetative growth, development or production of oxalic acid (one of this fungus’ secondary metabolites associated with disease) production. However, yhis does result in reduced fungal virulence. We show that, unexpectedly, the SsCM1 protein translocates to the host chloroplast, and demonstrated that this process is required for full fungal virulence. We have also determined that the fungal SsCM1 protein can interact with similar proteins produced by the host. In addition, we have shown that the fungal SsCM1 is able to suppress at least some of the effects imposed by reactive oxygen species which are produced as a defense mechanism by the host. Last, but not least, the results of our studies have provided evidence contradicting the current dogma on at least some of the mechanist aspects of how this pathogen infects the host. Contrary to previousons, indicating that this pathogen kills its host by use of metabolites and enzymes that degrade the host tissue (a process called necrotrophy), we now know that at least in the early phases of infection, the fungus interacts with live host tissue (a phenomenon known as biotrophy). Taken together, the results of our studies provide novel insights concerning the mechanistic aspects of Sclerotinia-host interactions. We hope this information will be used to interfere with the disease cycle in a manner that will protect plants from this devastating fungus.
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Sharon, Amir, and Maor Bar-Peled. Identification of new glycan metabolic pathways in the fungal pathogen Botrytis cinerea and their role in fungus-plant interactions. United States Department of Agriculture, 2012. http://dx.doi.org/10.32747/2012.7597916.bard.
Full textAbstract:
The involvement of glycans in microbial adherence, recognition and signaling is often a critical determinant of pathogenesis. Although the major glycan components of fungal cell walls have been identified there is limited information available on its ‘minor sugar components’ and how these change during different stages of fungal development. Our aim was to define the role of Rhacontaining-glycans in the gray mold disease caused by the necrotrophic fungus B. cinerea. The research was built on the discovery of two genes, Bcdhand bcer, that are involved in formation of UDP-KDG and UDP-Rha, two UDP- sugars that may serve as donors for the synthesis of cell surface glycans. Objectives of the proposed research included: 1) To determine the function of B. cinereaBcDh and BcEr in glycan biosynthesis and in pathogenesis, 2) To determine the expression pattern of BcDH and BcERand cellular localization of their encoded proteins, 3) Characterize the structure and distribution of Rha- containing glycans, 4) Characterization of the UDP-sugar enzymes and potential of GTs involved in glycanrhamnosylation. To address these objectives we generated a series of B. cinereamutants with modifications in the bchdhand bcergenes and the phenotype and sugar metabolism in the resulting strains were characterized. Analysis of sugar metabolites showed that changes in the genes caused changes in primary and secondary sugars, including abolishment of rhamnose, however abolishment of rhamnose synthesis did not cause changes in the fungal phenotype. In contrast, we found that deletion of the second gene, bcer, leads to accumulation of the intermediate sugar – UDP- KDG, and that such mutants suffer from a range of defects including reduced virulence. Further analyses confirmed that UDP-KDG is toxic to the fungus. Studies on mode of action suggested that UDP-KDG might affect integrity of the fungal cell wall, possibly by inhibiting UDP-sugars metabolic enzymes. Our results confirm that bcdhand bcerrepresent a single pathway of rhamnose synthesis in B. cinerea, that rhamnose does not affect in vitro development or virulence of the fungus. We also concluded that UDP-KDG is toxic to B. cinereaand hence UDP-KDG or compounds that inhibit Er enzymes and lead to accumulation of UDP-KDG might have antifungal activity. This toxicity is likely the case with other fungi, this became apparent in a collaborative work with Prof. Bart Thomma of Wageningen University, NETHERLANDS . We have shown the deletion of ER mutant in Verticillium dahlia gave plants resistance to the fungal infection.
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Alfano, James, Isaac Barash, Thomas Clemente, Paul E. Staswick, Guido Sessa, and Shulamit Manulis. Elucidating the Functions of Type III Effectors from Necrogenic and Tumorigenic Bacterial Pathogens. United States Department of Agriculture, January 2010. http://dx.doi.org/10.32747/2010.7592638.bard.
Full textAbstract:
Many phytopathogenic bacteria use a type III protein secretion system (T3SS) to inject type III effectors into plant cells. In the experiments supported by this one-year feasibility study we investigated type III effector function in plants by using two contrasting bacterial pathogens: Pseudomonas syringae pv. tomato, a necrotrophic pathogen and Pantoea agglomerans, a tumorigenic pathogen. The objectives are listed below along with our major conclusions, achievements, and implications for science and agriculture. Objective 1: Compare Pseudomonas syringae and Pantoea agglomerans type III effectors in established assays to test the extent that they can suppress innate immunity and incite tumorigenesis. We tested P. agglomerans type III effectors in several innate immunity suppression assays and in several instances these effectors were capable of suppressing plant immunity, outputs that are suppressed by P. syringae effectors. Interestingly, several P. syringae effectors were able to complement gall production to a P. agglomerans pthGmutant. These results suggest that even though the disease symptoms of these pathogens are dramatically different, their type III effectors may function similarly. Objective 2: Construct P. syringae mutants in different combinations of type III-related DNA clusters to reduce type III effector redundancy. To determine their involvement in pathogenicity we constructed mutants that lack individual and multiple type III-related DNA clusters using a Flprecombinase-mediated mutagenesis strategy. The majority of single effector mutants in DC3000 have weak pathogenicity phenotypes most likely due to functional redundancy of effectors. Supporting this idea, Poly-DNAcluster deletion mutants were more significantly reduced in their ability to cause disease. Because these mutants have less functional redundancy of type III effectors, they should help identify P. syringae and P. agglomerans effectors that contribute more significantly to virulence. Objective 3: Determine the extent that P. syringae and P. agglomerans type III effectors alter hormone levels in plants. Inhibition of auxin polar transport by 2,3,5-triiodobenzoic acid (TIBA) completely prevented gall formation by P. agglomerans pv. gypsophilae in gypsophila cuttings. This result supported the hypothesis that auxin and presumably cytokinins of plant origin, rather than the IAA and cytokinins secreted by the pathogen, are mandatory for gall formation. Transgenic tobacco with pthGshowed various phenotypic traits that suggest manipulation of auxin metabolism. Moreover, the auxin levels in pthGtransgenic tobacco lines was 2-4 times higher than the control plants. External addition of auxin or cytokinins could modify the gall size in gypsophila cuttings inoculated with pthGmutant (PagMx27), but not with other type III effectors. We are currently determining hormone levels in transgenic plants expressing different type III effectors. Objective 4: Determine whether the P. agglomerans effectors HsvG/B act as transcriptional activators in plants. The P. agglomerans type III effectors HsvG and HsvB localize to the nucleus of host and nonhost plants and act as transcription activators in yeast. Three sites of adjacent arginine and lysine in HsvG and HsvB were suspected to act as Nuclear localization signals (NLS) domains. A nuclear import assay indicated two of the three putative NLS domains were functional NLSs in yeast. These were shown to be active in plants by fusing HsvG and HsvB to YFP. localization to the nucleus was dependent on these NLS domains. These achievements indicate that our research plan is feasible and suggest that type III effectors suppress innate immunity and modulate plant hormones. This information has the potential to be exploited to improve disease resistance in agricultural crops.
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Xu, Jin-Rong, and Amir Sharon. Comparative studies of fungal pathogeneses in two hemibiotrophs: Magnaporthe grisea and Colletotrichum gloeosporioides. United States Department of Agriculture, May 2008. http://dx.doi.org/10.32747/2008.7695585.bard.
Full textAbstract:
Plant pathogenic fungi have various life styles and different plant infection strategies. Hemibiotrophs like Magnaporthe grisea and Colletotrichum species develop specialized structures during plant infection. The goal of this study was to identify, characterize, and compare genes required for plant infection in M. grisea and C. gloeosporioides. Specific objectives are to: 1) further characterize genes identified in the preliminary studies of C. gloeosporioides and M. grisea;2) identify and characterize additional fungal genes tagged by GFP; and 3) identify in planta growth and appressorium-specific genes by subtractive hybridization and transcript profiling by the LongSAGE method. In this study, the PI and Co-PI collaborated closely on studies in M. grisea and C. gloeosporioides. In M. grisea, REMI and ATMT were used to transform the wildtype with promoter-less EGFP constructs. A total of 28 mutants defective in different plant infection processes or expressing EGFP during plant infection were identified. Genes disrupted in five selected mutants have been identified, including MG03295 that encodes a putative Rho GTPase. In transformant L1320, the transforming vector was inserted in the MIRI gene that encodes a nuclear protein. The expression of MIRI was highly induced during infection. Deletion and site-directed mutagenesis analyses were used to identify the promoter regions and elements that were essential for induced in planta expression of MIRI. This was the first detailed characterization of the promoter of an in planta gene in M. grisea and the MIRI promoter can be used to monitor infectious growth. In addition, the Agilent whole-genome array of M. grisea was used for microarray analyses with RNA samples from appressoria formed by the wild-type shain and the pmkl and mstl2 mutants. Over 200 genes were downregulated in the mst I 2 and pmkl mutants. Some of them are putative transcription factors that may regulate appressorium formation and infectious hyphal growth. In C. gloeosporioides, various REMI mutants showing different pathogenic behavior were identified and characterized. Mutants N3736 had a single insertion and was hyper-virulent. The gene disrupted in mutant3736 (named CgFMOI) encodes a FAD-dependent monooxygenase. Expression analyses linked the expression of the CgFMOI gene with the necrotrophic phase of fungal infection, and also suggest that expression of CgFMOl is unnecessary for the first stages of infection and for biotrophy establishment. All CgFMOl-silenced mutants had reduced virulence. In REMI mutant N159, the tagged gene encodes a putative copper transporter that is homologue of S. cerevisiae CTR2. In yeast, Ctr2 is a vacuolar transporter for moving copper from the vacuole to the cytoplasm. The gene was therefore termed CgCTR2. In addition to characterization of CgCTR2, we also conducted comparative analyses in M. grisea. The M. grisea CgCTR-2 homolog was isolated, knockout strains were generated and characterized and the M. grisea was used to complement the Nl 59 C. gloeosporioides mutant. Overall, we have accomplished most of proposed experiments and are in the process of organizing and publishing other data generated in this project. For objective 3, we used the microarray analysis approach. Several genes identified in this study are novel fungal virulence factors. They have the potential to be used as targets for developing more specific or effective fungicides. In the long run, comparative studies of fungal genes, such as our CgCTR2 work, may lead to better disease control strategies.
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Granot, David, Richard Amasino, and Avner Silber. Mutual effects of hexose phosphorylation enzymes and phosphorous on plant development. United States Department of Agriculture, January 2006. http://dx.doi.org/10.32747/2006.7587223.bard.
Full textAbstract:
Research objectives 1) Analyze the combined effects of hexose phosphorylation and P level in tomato and Arabidopsis plants 2) Analyze the combined effects of hexose phosphorylation and P level in pho1 and pho2 Arabidopsis mutants 3) Clone and analyze the PHO2 gene 4) Select Arabidopsis mutants resistant to high and low P 5) Analyze the Arabidopsis mutants and clone the corresponding genes 6) Survey wild tomato species for growth characteristics at various P levels Background to the topic Hexose phosphorylating enzymes, the first enzymes of sugar metabolism, regulate key processes in plants such as photosynthesis, growth, senescence and vascular transport. We have previously discovered that hexose phosphorylating enzymes might regulate these processes as a function of phosphorous (P) concentration, and might accelerate acquisition of P, one of the most limiting nutrients in the soil. These discoveries have opened new avenues to gain fundamental knowledge about the relationship between P, sugar phosphorylation and plant development. Since both hexose phosphorylating enzymes and P levels affect plant development, their interaction is of major importance for agriculture. Due to the acceleration of senescence caused by the combined effects of hexose phosphorylation and P concentration, traits affecting P uptake may have been lost in the course of cultivation in which fertilization with relatively high P (30 mg/L) are commonly used. We therefore intended to survey wild tomato species for high P-acquisition at low P soil levels. Genetic resources with high P-acquisition will serve not only to generate a segregating population to map the trait and clone the gene, but will also provide a means to follow the trait in classical breeding programs. This approach could potentially be applicable for other crops as well. Major conclusions, solutions, achievements Our results confirm the mutual effect of hexose phosphorylating enzymes and P level on plant development. Two major aspects of this mutual effect arose. One is related to P toxicity in which HXK seems to play a major role, and the second is related to the effect of HXK on P concentration in the plant. Using tomato plants we demonstrated that high HXK activity increased leaf P concentration, and induced P toxicity when leaf P concentration increases above a certain high level. These results further support our prediction that the desired trait of high-P acquisition might have been lost in the course of cultivation and might exist in wild species. Indeed, in a survey of wild species we identified tomato species that acquired P and performed better at low P (in the irrigation water) compared to the cultivated Lycopersicon esculentum species. The connection between hexose phosphorylation and P toxicity has also been shown with the P sensitive species VerticordiaplumosaL . in which P toxicity is manifested by accelerated senescence (Silber et al., 2003). In a previous work we uncovered the phenomenon of sugar induced cell death (SICD) in yeast cells. Subsequently we showed that SICD is dependent on the rate of hexose phosphorylation as determined by Arabidopsis thaliana hexokinase. In this study we have shown that hexokinase dependent SICD has many characteristics of programmed cell death (PCD) (Granot et al., 2003). High hexokinase activity accelerates senescence (a PCD process) of tomato plants, which is further enhanced by high P. Hence, hexokinase mediated PCD might be a general phenomena. Botrytis cinerea is a non-specific, necrotrophic pathogen that attacks many plant species, including tomato. Senescing leaves are particularly susceptible to B. cinerea infection and delaying leaf senescence might reduce this susceptibility. It has been suggested that B. cinerea’s mode of action may be based on induction of precocious senescence. Using tomato plants developed in the course of the preceding BARD grant (IS 2894-97) and characterized throughout this research (Swartzberg et al., 2006), we have shown that B. cinerea indeed induces senescence and is inhibited by autoregulated production of cytokinin (Swartzberg et al., submitted). To further determine how hexokinase mediates sugar effects we have analyzed tomato plants that express Arabidopsis HXK1 (AtHXK1) grown at different P levels in the irrigation water. We found that Arabidopsis hexokinase mediates sugar signalling in tomato plants independently of hexose phosphate (Kandel-Kfir et al., submitted). To study which hexokinase is involved in sugar sensing we searched and identified two additional HXK genes in tomato plants (Kandel-Kfir et al., 2006). Tomato plants have two different hexose phosphorylating enzymes; hexokinases (HXKs) that can phosphorylate either glucose or fructose, and fructokinases (FRKs) that specifically phosphorylate fructose. To complete the search for genes encoding hexose phosphorylating enzymes we identified a forth fructokinase gene (FRK) (German et al., 2004). The intracellular localization of the four tomato HXK and four FRK enzymes has been determined using GFP fusion analysis in tobacco protoplasts (Kandel-Kfir et al., 2006; Hilla-Weissler et al., 2006). One of the HXK isozymes and one of the FRK isozymes are located within plastids. The other three HXK isozymes are associated with the mitochondria while the other three FRK isozymes are dispersed in the cytosol. We concluded that HXK and FRK are spatially separated in plant cytoplasm and accordingly might play different metabolic and perhaps signalling roles. We have started to analyze the role of the various HXK and FRK genes in plant development. So far we found that LeFRK2 is required for xylem development (German et al., 2003). Irrigation with different P levels had no effect on the phenotype of LeFRK2 antisense plants. In the course of this research we developed a rapid method for the analysis of zygosity in transgenic plants (German et al., 2003).