Academic literature on the topic 'Fungal adhesion'

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Journal articles on the topic "Fungal adhesion"

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Jones, E. B. Gareth. "Fungal adhesion." Mycological Research 98, no. 9 (September 1994): 961–81. http://dx.doi.org/10.1016/s0953-7562(09)80421-8.

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Essen, Lars-Oliver, Marian Samuel Vogt, and Hans-Ulrich Mösch. "Diversity of GPI-anchored fungal adhesins." Biological Chemistry 401, no. 12 (November 26, 2020): 1389–405. http://dx.doi.org/10.1515/hsz-2020-0199.

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AbstractSelective adhesion of fungal cells to one another and to foreign surfaces is fundamental for the development of multicellular growth forms and the successful colonization of substrates and host organisms. Accordingly, fungi possess diverse cell wall-associated adhesins, mostly large glycoproteins, which present N-terminal adhesion domains at the cell surface for ligand recognition and binding. In order to function as robust adhesins, these glycoproteins must be covalently linkedto the cell wall via C-terminal glycosylphosphatidylinositol (GPI) anchors by transglycosylation. In this review, we summarize the current knowledge on the structural and functional diversity of so far characterized protein families of adhesion domains and set it into a broad context by an in-depth bioinformatics analysis using sequence similarity networks. In addition, we discuss possible mechanisms for the membrane-to-cell wall transfer of fungal adhesins by membrane-anchored Dfg5 transglycosidases.
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Lipke, Peter N., Caleen Ramsook, Melissa C. Garcia-Sherman, Desmond N. Jackson, Cho X. J. Chan, Michael Bois, and Stephen A. Klotz. "Between Amyloids and Aggregation Lies a Connection with Strength and Adhesion." New Journal of Science 2014 (February 2, 2014): 1–12. http://dx.doi.org/10.1155/2014/815102.

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We tell of a journey that led to discovery of amyloids formed by yeast cell adhesins and their importance in biofilms and host immunity. We begin with the identification of the adhesin functional amyloid-forming sequences that mediate fiber formation in vitro. Atomic force microscopy and confocal microscopy show 2-dimensional amyloid “nanodomains” on the surface of cells that are activated for adhesion. These nanodomains are arrays of adhesin molecules that bind multivalent ligands with high avidity. Nanodomains form when adhesin molecules are stretched in the AFM or under laminar flow. Treatment with anti-amyloid perturbants or mutation of the amyloid sequence prevents adhesion nanodomain formation and activation. We are now discovering biological consequences. Adhesin nanodomains promote formation and maintenance of biofilms, which are microbial communities. Also, in abscesses within candidiasis patients, we find adhesin amyloids on the surface of the fungi. In both human infection and a Caenorhabditis elegans infection model, the presence of fungal surface amyloids elicits anti-inflammatory responses. Thus, this is a story of how fungal adhesins respond to extension forces through formation of cell surface amyloid nanodomains, with key consequences for biofilm formation and host responses.
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Douglas, L. Julia. "Adhesin - receptor interactions in the attachment ofCandida albicansto host epithelial cells." Canadian Journal of Botany 73, S1 (December 31, 1995): 1147–53. http://dx.doi.org/10.1139/b95-371.

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The ability of Candida albicans to adhere to a variety of host surfaces is thought to be an important factor in the pathogenesis of candidosis. Adhesion of the yeast form of the fungus to epithelial cells can involve several kinds of adhesion – receptor interaction. Yeast adhesins are typically mannoproteins associated with fibrils or fimbriae on the fungal surface. Lectinlike interactions have been identified between the protein portion of two mannoprotein adhesins and glycosides containing L-fucose or N-acetylglucosamine. The fucoside-binding adhesin has been purified and shown to have an affinity for glycosphingolipid receptors carrying the H blood-group antigen. A fimbrial adhesin has also been described that binds to gangliosides containing a βGalNAc(1–4)βGal disaccharide sequence. Other mannoprotein adhesins proposed recently include the factor 6 epitope present on serotype A strains of C. albicans and an integrin analogue. Adhesin expression appears to be regulated by a number of environmental signals, including osmolarity and the availability of iron and sugars. Additional adhesion-dependent signals might trigger further responses such as the initiation of morphogenesis. Key words: Candida albicans, yeast adhesion, epithelial cell adhesion.
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Upadhyay, Santosh Kumar, Lakshna Mahajan, Sandhya Ramjee, Yogendra Singh, Seemi Farhat Basir, and Taruna Madan. "Identification and characterization of a laminin-binding protein of Aspergillus fumigatus: extracellular thaumatin domain protein (AfCalAp)." Journal of Medical Microbiology 58, no. 6 (June 1, 2009): 714–22. http://dx.doi.org/10.1099/jmm.0.005991-0.

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Aspergillus fumigatus, an opportunistic fungal pathogen, infects the human host via inhalation of airborne conidia. Adhesion of fungal conidia, to host cells and extracellular matrix (ECM) components associated with host tissue surfaces, is thought to be the primary step in the pathogenesis and dissemination of infection. To identify novel adhesion proteins (adhesins) of A. fumigatus, we screened its proteome in silico using spaan (software program for prediction of adhesins and adhesin-like proteins using neural networks). One of the predicted adhesin-encoding genes with a P ad (probability of being adhesin) value >0.9, the gene encoding extracellular thaumatin domain protein (AfCalA), was cloned and expressed in Escherichia coli. Recombinant AfCalAp showed significant binding with laminin and murine lung cells. Anti-AfCalAp antibodies inhibited the binding of AfCalAp to laminin in a dose-dependent manner. Significant binding of anti-AfCalAp antibodies to 2 h swollen conidia suggests the presence of AfCalAp on the conidial surface. AfCalA transcript was not detectable in resting conidia but was detected in conidia incubated with RPMI 1640 medium in the presence and absence of lung epithelial cell line (A539)-derived ECM. Elevated levels of IgE antibodies specific to AfCalAp were observed in the sera of two out of seven patients with allergic bronchopulmonary aspergillosis. The study confirms the relevance of the bioinformatic approach for predicting fungal adhesins and establishes AfCalAp as a novel laminin-binding protein of A. fumigatus.
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Harrison, S. J., S. T. Moss, and E. B. G. Jones. "Fungal adhesion in aquatic hyphomycetes." International Biodeterioration 24, no. 4-5 (January 1988): 271–76. http://dx.doi.org/10.1016/0265-3036(88)90011-5.

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Gerin, P., M. N. Bellon-Fontaine, M. Asther, and P. G. Rouxhet. "Immobilization of fungal spores by adhesion." Biotechnology and Bioengineering 47, no. 6 (September 20, 1995): 677–87. http://dx.doi.org/10.1002/bit.260470608.

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Reinmets, Kristina, Amin Dehkharghani, Jeffrey S. Guasto, and Stephen M. Fuchs. "Microfluidic quantification and separation of yeast based on surface adhesion." Lab on a Chip 19, no. 20 (2019): 3481–89. http://dx.doi.org/10.1039/c9lc00275h.

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Fungal adhesion is fundamental to processes ranging from infections to food production. We developed a microfluidic assay for rapid screening and fractionation of genetically-related yeast based on adhesive properties.
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Filonow, Alexander B. "Germination and adhesion of fungal conidia on polycarbonate membranes and on apple fruit exposed to mycoactive acetate esters." Canadian Journal of Microbiology 49, no. 2 (February 1, 2003): 130–38. http://dx.doi.org/10.1139/w03-019.

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The adhesion and germination of conidia of nine fungal species were assessed on polycarbonate membranes or on the skin of apple fruit in sealed glass bottles injected or not injected with acetate esters. Adhesion was determined after dislodging conidia from surfaces using a sonication probe. Adhesion and germination of conidia of Aspergillus flavus, Aspergillus fumigatus, Aspergillus niger, Penicillium citrinum, Penicillium claviforme, or Trichoderma sp. on membranes after 48 h were not increased in a 1.84 μg mL–1headspace of butyl acetate (BA), ethyl acetate, hexyl acetate, 2-methylbutyl acetate, pentyl acetate, or propyl acetate. Adhesion and germination of Botrytis cinerea, Penicillium expansum, and Penicillium roquefortii conidia were stimulated by all esters. Only conidia of B. cinerea and P. expansum exhibited increased adhesion and germination on the skin of apple fruit in bottles exposed to 0.92 μg mL–1of BA. Only conidia of B. cinerea and P. expansum produced decay in inoculated puncture wounds on fruit. Freshly made puncture wounds or 24-h-old puncture wounds in fruit were more adhesive than the unpunctured skin of fruit to conidia of B. cinerea or P. expansum. Fresh wounds were more adhesive to both fungi than 24-h-old puncture wounds. The skin and wounds of fruit were as adhesive to B. cinerea conidia as they were to P. expansum conidia. A 4-h exposure to 1.43 μg mL–1of BA increased adhesion of B. cinerea and P. expansum conidia in 24-h-old wounds. Results suggest that acetate–ester stimulation most likely is not a rare phenomenon in the fungi. For nutrient-dependent decay pathogens of apple fruit, acetate esters may be an alternative chemical cue used to maintain adhesion of conidia to wound surfaces.Key words: spore adhesion, spore germination, mycoactive compounds.
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Chan, Cho X. J., and Peter N. Lipke. "Role of Force-Sensitive Amyloid-Like Interactions in Fungal Catch Bonding and Biofilms." Eukaryotic Cell 13, no. 9 (March 28, 2014): 1136–42. http://dx.doi.org/10.1128/ec.00068-14.

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ABSTRACTTheCandida albicansAls adhesin Als5p has an amyloid-forming sequence that is required for aggregation and formation of model biofilms on polystyrene. Because amyloid formation can be triggered by force, we investigated whether laminar flow could activate amyloid formation and increase binding to surfaces. ShearingSaccharomyces cerevisiaecells expressing Als5p orC. albicansat 0.8 dyne/cm2increased the quantity and strength of cell-to-surface and cell-to-cell binding compared to that at 0.02 dyne/cm2. Thioflavin T fluorescence showed that the laminar flow also induced adhesin aggregation into surface amyloid nanodomains in Als5p-expressing cells. Inhibitory concentrations of the amyloid dyes thioflavin S and Congo red or a sequence-specific anti-amyloid peptide decreased binding and biofilm formation under flow. Shear-induced binding also led to formation of robust biofilms. There was less shear-activated increase in adhesion, thioflavin fluorescence, and biofilm formation in cells expressing the amyloid-impaired V326N-substituted Als5p. Similarly,S. cerevisiaecells expressing Flo1p or Flo11p flocculins also showed shear-dependent binding, amyloid formation, biofilm formation, and inhibition by anti-amyloid compounds. Together, these results show that laminar flow activated amyloid formation and led to enhanced adhesion of yeast cells to surfaces and to biofilm formation.
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Dissertations / Theses on the topic "Fungal adhesion"

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Singleton, Ian. "The biosorption of particulates and metal ions by fungal mycelium." Thesis, University of Sheffield, 1989. http://etheses.whiterose.ac.uk/6033/.

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Particulate adsorption by Mucor flavus and Neurospora crassa is a physical property of the cell wall, independent of both cellular metabolism and the production of extracellular polymers. Initial attractive forces responsible for particulate adsorption by N. crassa are mainly electrostatic in nature and this mechanism probably holds for M. flavus also. The outer glucan layer of the cell wall of N. crassa, although able to adsorb particulates, was not as efficient as the underlying protein layer at particle adsorption. Young, growing mycelium generally adsorbs the , -, largest amount of particles, due to the continued production of adsorption sites and the entrapment of particulates by hyphae. Factors increasing adsorption include nutrient starvation of mycelium and incubation with low concentrations of magnesium ions. Relatively high concentrations of mercury and copper ions decrease adsorption perhaps due to the precipitation and adsorption of the corresponding metal sulphides on the mycelial surface thereby effectively physically interfering with further particulate adsorption. Optimum conditions for adsorption are a temperature of 250C and a slightly acid pH value. Also, small particles are more readily adsorbed than large particles. Mucor flavus can adsorb clays and this ability may be used to treat industrial effluents which contain large amounts of clay minerals. An acid pH and a temperature of 250C are optimum conditions for clay adsorption by the fungus. Low concentrations of montmorillonite and kaolinite increase biomass production by Aspergillus niger in submerged culture, due to the inhibition of pellet formation by the fungus. The clays cause A. niger to grow in a more filamentous form and presumably would affect other fungi in a similar way. The use of clays to control fungal morphology may be important in several industrial fermentations. Low concentrations of the fungicide thiram stimulated the growth of Aspergillus niger in the presence of montmorillonite. Immobilization of fungi by magnetic means is possible due to their ability to adsorb magnetite. This method could also be used to remove fungi from fermentation media as an alternative to filtration or centrifugation. Even though older hyphae of Penicillium chrysogenum are unable to adsorb magnetite, this fungus can still be magnetically immobilized if it is grown from a spore suspension in the presence of magnetite. Either the spores or young hyphae of this fungus adsorb magnetite, producing pellets with magnetic properties. Magnetite adsorption occurs optimally at a temperature of 250C and is constant over a wide range of pH values. Waste mycelium of A. niger from the surface fermentation method of citric acid production can be magnetically removed from solution after adsorbing magnetite. Dilute solutions of sodium hydroxide and sodium bicarbonate desorbed magnetite attached to mycelial surfaces. Silver is accumulated selectively by A. niger waste mycelium produced by the surface fermentation method of citric acid production. The process is rapid, maximum uptake occurring twenty minutes after initial exposure of the mycelium to a silver solution. Silver accumulation by the mycelium is relatively insensitive to changes in pH and temperature, a slight decrease in uptake only occurring at a temperature of 800C. Dilute solutions of H2S04 and HNO3 desorb silver from the mycelial surface. However, this process is relatively inefficient and more effective desorbents need to be found to make the silver accumulation process economically viable.
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Hobden, Carole Lesley. "A study of the cell surface properties of Candida albicans." Thesis, University of Essex, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.295552.

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Kim, Ah-Ram. "Experimental and theoretical investigation of the role of nanofibrous topography feature size on adhesion of Candida albicans." Thesis, Virginia Tech, 2015. http://hdl.handle.net/10919/73314.

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Biofilm formation on medical devices is responsible for a substantial portion of healthcare associated infections with approximately 99,000 deaths and estimated financial burden of $28-$45 billion annually. Given the long-standing challenges of biofilm eradication, physical and chemical surface modifications to prevent biofilm formation from the early adhesion stage, continue to gain momentum. Nanoscale structural features, ubiquitous in both natural and synthetic surfaces, are increasingly recognized to have wide-ranging effects on microorganism adhesion and biofilm development. In this thesis, bio-inspired nanofiber-coated polystyrene surfaces were developed to systematically investigate how highly ordered surface nanostructures (200nm-2000nm in size) impact adhesion and proliferation of model fungal pathogen, Candida albicans. A theoretical model for cell-textured surface interaction was also developed using thermodynamic principles to demonstrate that single cell adhesion to surface can be used to describe the population behavior. The trend for adhesion density of C. albicans on nanofiber-textured surfaces of varying diameters correlates with our theoretical finding of adherent single-cell energetic state. Findings from this thesis can be used for enhanced ab initio design of antifouling surfaces for medical applications and beyond. We demonstrate a successful prototypical example of reduction in biofilm formation by optimally designed nanofiber coating of urinary catheters.
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Jain, Charu. "Development of a fungal virulence assay using Caenorhabditis elegans as a model host to identify mechanisms of host pathogen interactions." Digital WPI, 2012. https://digitalcommons.wpi.edu/etd-dissertations/149.

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Candida albicans is an opportunistic pathogen, which is responsible for causing systemic infection in immunocompromised patients in hospital settings (nosocomial infections). 90% of these nosocomial fungal infections are caused by C. albicans, and the estimated annual cost of treating them exceeds $1 billion per year. Despite this expenditure, there is a high mortality rate of 50%. There are two main routes of infections, first a mucosal infection that can spread and invades deeper into the tissues and gets disseminated into the bloodstream. Second, more frequently seen in hospital settings, is when Candida cells dislodge from a biofilm that has formed on intravenous devices or catheters. Treatment of these diseases is difficult due to a dearth of antifungal drugs and new strategies are required to explore mechanisms used by Candida in causing infection. One way of approaching these significant scientific challenges is to identify virulence determinants and mechanisms, which apart from providing insightful knowledge of fungal pathogenesis, can also be used as targets for antifungal drug development. The innate immune responses in humans, which are important for defense against fungal infections, are conserved in Caenorhabditis elegans. In order to identify Candida virulence factors, I have developed a C. elegans based pathogenesis assay, where nematodes were infected with fungi (both S. cerevisiae and C. albicans) and observed for disease phenotypes including death. This assay can be used to study several aspects of disease progression in worms from swelling (inflammation a bio-marker of infection) to colonization in the intestine, leading to intestinal distension and ultimately death of the host worm. The assay offers a fast and simple way of identifying unknown genes, which when established as a virulence determinant in the worm model, can be further studied in mammalian models. I demonstrate the utility of this assay in multiple ways. First as proof of principle using this assay I have identified a fungal mutant cap1, which is susceptible to reactive oxygen species (ROS), and fails to cause disease, except in bli-3 mutant worms that carry a mutation in an oxidase gene and is responsible for the oxidative stress. Second, we screened a library of ~1200 C. albicans mutants, and identified 7 genes, 3 known (CMP1, IFF11 and SAP 8), validating the assay and 4 novel genes (orf19.1219, orf19.6713, DOT4 and ZCF15) that play a role in fungal infection. Third use of this assay is to test potential drugs in a high throughput fashion. Families of related compounds were identified through a screen of 30,000 compounds, for their ability as potential inhibitors of C. albicans adhesion to biological and inert surfaces. These compounds were further tested in this assay for their ability to reduce infection of C. albicans in worms. The assay provides us with a method to test efficacy of antifungals in vivo. Finally, using the survival assay, a test for mortality caused by infection, we can observe disparity in the different C. albicans fluconazole resistant strains isolated from AIDS patients. In addition this assay after small modification can be potentially employed to screen the C. elegans RNAi library to identify the modulators of innate immune responses during fungal infection.
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Bain, Judith M. "Contribution of glycosylation to the structure and properties of the Candida albicans cell wall." Thesis, University of Aberdeen, 2002. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU159710.

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Adhesion of the opportunistic fungal pathogen, Candida albicans, to host surfaces is mediated through the mannoprotein-rich surface. This thesis examines the role of cell wall mannoproteins in the host-fungus interactions and the mechanism by which these proteins are tethered to the major structural polysaccharides of the wall. The mannosyl modifications of cell surface proteins are involved in host interaction. Periodate oxidation of fungal surface carbohydrates reduced adhesion to epithelial cells confirming that mannan is a component adhesion of C. albicans. Strains of C. albicans disrupted in MNT1, 2 and 3 genes encoding mannosyl transferases, were reduced in adhesion to both epithelial cells and Matrigel. Adhesion was also influenced by the Ura-status of C. albicans strains, which differs as a result of targeted gene disruption by the URA-blaster strategy. Ura-strains were less adhesive but this was not due to altered growth rate and could not be alleviated by adding excess uridine. Therefore current methods for gene deletion have to be questioned when considering adhesion as a virulence factor. Strains defective in glycosylation were altered in covalently associated cell wall proteins (CWPs) in terms of mobility during electrophoresis. The greatest alterations observed were in the CWPs of C. albicans strains with severe glycosylation defects, such as in Dochl/Doch1 and Dpmt1/Dpmt1 mutants, defective in N- and O-linked glycosylation, respectively. These strains also secreted more mannoprotein were altered in morphology or gross cell wall structure, and had elevated cell wall chitin. Therefore glycosylation is required for normal CWP incorporation and cell wall construction. For the first time C. albicans was shown to link a CWP, other than Pir-CWP, to the cell wall network via an alkali-sensitive linkage. The nature of this type of linkage remains unknown, however an O-mannan chain, whose synthesis is not initiated by Pmt1p, may be involved. Pir-CWP incorporation was increased in a Dpmt1/Dpmt1 null mutant and could be partially attributed to increased expression. Pir-CWP expression and incorporation was pH-dependent and may be regulated in response to the different pH at different host niches.
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Chan, Sin-yee Joanna, and 陳善怡. "The study of potential adhesion factors of penicillium marneffei." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B44524651.

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Jones, Rhian. "Structural and functional characterisation of adhesin and effector proteins from pathogenic fungi." Thesis, Imperial College London, 2015. http://hdl.handle.net/10044/1/58140.

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This PhD has focussed on characterising two proteins key to fungal infections; the Als adhesins and BEC1054. The Als (agglutinin-like sequence) family of surface adhesins are critical virulence factors from Candida albicans, contributing to biofilm formation and colonisation of a range of tissues in the human host. The broad tissue tropism of Als has been linked to a broadly specific peptide binding cavity (pbc) identified in crystal structures of Als N-terminal domains (NTs). Questions remained regarding the relative roles of the pbc and Als aggregative mechanisms in host cell binding. A series of targeted mutants generated in Als3 were characterised in vitro via NMR and in vivo (collaborator’s work) to delineate these adhesion mechanisms and demonstrate that the pbc alone mediates host binding. It was further demonstrated that sequence differences in the pbcs of Als1 and 3 underlie differences in Als substrate binding specificities. Solution based assays showed that Als3 binds to a wider range of peptide sequences; correlating with a larger pbc and additional interactions with peptides formed in Als-peptide co-crystal structures. We hypothesise that the broader binding specificity of Als3 correlates with the protein’s increased contribution to C. albicans adhesion and virulence in infection. Binding assays provided new insights into the peptide binding mechanism, and a robust system for future development of novel Als inhibitors. Following infection of barley, Blumeria graminis delivers effector proteins such as BEC1054 into the plant to perturb host immunity. The crystal structure of BEC1054 was solved, revealing an RNAse fold that lacks catalytic residues required for hydrolysis. Binding to nucleic acid has been demonstrated, and the binding site localised via mapping of chemical shift perturbations (CSPs) in NMR. Preliminary data have been acquired to test the theory that BEC could associate with ribosomes. Understanding the role of BEC1054 could provide important insights into effector-based modulation of plant immunity, an area that is currently poorly understood.
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Holder, Diane J. "Adhesion properties and cell surface characteristics of the entomopathogenic fungus Beauveria bassiana a link between morphology and virulence /." [Gainesville, Fla.] : University of Florida, 2005. http://purl.fcla.edu/fcla/etd/UFE0011221.

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Emerson, Ray Jenkins. "Microbial Adhesion to Medical Implant Materials: An Atomic Force Microscopy Study." Link to electronic thesis, 2004. http://www.wpi.edu/Pubs/ETD/Available/etd-0209104-162349.

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Tran, Van Tuan [Verfasser], Susanna [Akademischer Betreuer] Braus-Stromeyer, Gerhard [Akademischer Betreuer] Braus, Stefanie [Akademischer Betreuer] Pöggeler, and Stefan [Akademischer Betreuer] Irniger. "Adhesion of the rapeseed pathogen Verticillium longisporum to its host Brassica napus: Uncovering adhesion genes and the evolutionary origin of the fungus / Van Tuan Tran. Gutachter: Gerhard Braus ; Stefanie Pöggeler ; Stefan Irniger. Betreuer: Susanna Braus-Stromeyer." Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2011. http://d-nb.info/1044051426/34.

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Books on the topic "Fungal adhesion"

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Odds, Frank C. Pathogenesis of fungal disease. Edited by Christopher C. Kibbler, Richard Barton, Neil A. R. Gow, Susan Howell, Donna M. MacCallum, and Rohini J. Manuel. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780198755388.003.0008.

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The pathogenesis of fungal disease involves an interplay between fungal virulence factors and host immune responses. Most fungal pathogens are opportunists that preferentially invade hosts with immune defects, but the fact that relative pathogenicity varies between fungal species (and even between different strains within a species) is evidence that fungi have evolved multiple, different molecular virulence factors. Experiments in which genes encoding putative virulence attributes are specifically disrupted and the resulting mutants are tested for virulence in a range of vertebrate and invertebrate hosts have identified or confirmed many gene products as significant for the pathogenesis of various types of fungal disease. These include factors determining fungal shape in vivo, biofilm formation, and a plethora of surface components, including adhesins and hydrolytic enzymes. This chapter provides an overview of fungal virulence attributes.
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Book chapters on the topic "Fungal adhesion"

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Nicholson, Ralph L. "Adhesion of Fungal Propagules." In Developments in Plant Pathology, 117–34. Dordrecht: Springer Netherlands, 1996. http://dx.doi.org/10.1007/978-94-009-0189-6_7.

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Nicholson, Ralph L., and Lynn Epstein. "Adhesion of Fungi to the Plant Surface." In The Fungal Spore and Disease Initiation in Plants and Animals, 3–23. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4899-2635-7_1.

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Braun, E. J., and R. J. Howard. "Adhesion of fungal spores and germlings to host plant surfaces." In The Protistan Cell Surface, 202–12. Vienna: Springer Vienna, 1994. http://dx.doi.org/10.1007/978-3-7091-9378-5_11.

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Kennedy, Michael J. "Candida Blastospore Adhesion, Association, and Invasion of the Gastrointestinal Tract of Vertebrates." In The Fungal Spore and Disease Initiation in Plants and Animals, 157–80. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4899-2635-7_7.

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Zordan, Rebecca, and Brendan Cormack. "Adhesins in Opportunistic Fungal Pathogens." In Candida and Candidiasis, 243—P2. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555817176.ch16.

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Calderone, R. A. "Multifunctional Adhesins in Yeasts." In Fungal Cell Wall and Immune Response, 365–73. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76074-7_27.

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Castaño, Irene, Alejandro De Las Peñas, and Brendan P. Cormack. "Function and Regulation of Adhesin Gene Families in Saccharomyces cerevisiae, Candida albicans, and Candida glabrata." In Molecular Principles of Fungal Pathogenesis, 163–75. Washington, DC, USA: ASM Press, 2014. http://dx.doi.org/10.1128/9781555815776.ch11.

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Epstein, Lynn, and Ralph L. Nicholson. "Adhesion and Adhesives of Fungi and Oomycetes." In Biological Adhesives, 41–62. Berlin, Heidelberg: Springer Berlin Heidelberg, 2006. http://dx.doi.org/10.1007/978-3-540-31049-5_3.

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Epstein, Lynn, and Ralph Nicholson. "Adhesion and Adhesives of Fungi and Oomycetes." In Biological Adhesives, 25–55. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46082-6_2.

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Mazzoli, Roberto, and Enrica Pessione. "Ancient Textile Deterioration and Restoration: Bio-Cleaning of an Egyptian Shroud Held in the Torino Museum." In Microorganisms in the Deterioration and Preservation of Cultural Heritage, 199–216. Cham: Springer International Publishing, 2021. http://dx.doi.org/10.1007/978-3-030-69411-1_9.

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AbstractAncient textiles are fragile and several factors can affect their integrity. In the present chapter, the main agents of deterioration of old and new textiles, namely physical-chemical (light, oxygen, heat, and humidity) and biological factors as well as human erroneous interventions will be explored. As far as the biological deterioration is considered, the effects of microbial growth, primary and secondary metabolites (acids, solvents, surfactants, pigments) and enzymes (lipases, proteases, and glycosidases) on textile strength and cleanliness will be described in details. The main fungal and bacterial species involved in the damage (textile discoloration, black and green spots, cuts) will be reported. Adhesive application during restoration procedures is discussed to highlight the risk of glue thickening giving rise to dull precipitates on the fabric.The main strategies for oil-stain and glue removal (both animal glue, such as fish collagen, and vegetal glue, i.e. starch) will be described in the paragraph devoted to biorestoration. Finally, a case study concerning an ancient Coptic tunic housed in the Egyptian Museum of Torino, Italy, and biocleaned by means of gellan-immobilized alpha-amylase from Bacillus sp. will be largely discussed by reporting historical data, adhesive characterization, methods for artificial aging of simulated sample and glue removal from the artwork.
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Conference papers on the topic "Fungal adhesion"

1

Gulati, Deepaksh, and Mohini Sain. "Effect of Fungal Modification on Fiber-Matrix Adhesion in Natural Fiber Reinforced Polymer Composites." In SAE 2006 World Congress & Exhibition. 400 Commonwealth Drive, Warrendale, PA, United States: SAE International, 2006. http://dx.doi.org/10.4271/2006-01-0006.

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2

Katola, Viktor. "MICROSCOPIC FUNGI, THEIR EVOLUTION, ROLE IN NATURE AND IN HUMAN PATHOLOGY." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9d9097a9.40840282.

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A brief outline of the evolution of microscopic fungi, structure, chemical composition and role in nature. Attention is paid to adhesins of the cell surface of fungi that determine their colonization and the development of infectious pathology
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