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Academic literature on the topic 'Bacterial wall'

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Published: 25 May 2024

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Journal articles on the topic "Bacterial wall"

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Singh, Adya P. "Certain Aspects of Bacterial Degradation of Pinus Radiata Wood." IAWA Journal 10, no. 4 (1989): 405–15. http://dx.doi.org/10.1163/22941932-90001132.

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Bacterial degradation of tracheid walls of Pinus radiata wood was examined by transmission electron microscopy. The wall degradation appeared to be of two different forms, one where bacteria were present within tracheid walls forming tunnels as they moved - tunnelling type of degradation, and the other where bacteria degraded the wall from the lumen outwards - erosion type of degradation. The residual material arising from bacterial erosion of the tracheid wall spread to various extents into the lumen and contained mixed bacterial populations of varied forms. Microscopic details of these two degradation forms which involved adjoining wall areas of the same tracheid are described.
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Singh, Adya P., Yoon Soo Kim, and Ramesh R. Chavan. "Relationship of wood cell wall ultrastructure to bacterial degradation of wood." IAWA Journal 40, no. 4 (November 16, 2019): 845–70. http://dx.doi.org/10.1163/22941932-40190250.

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ABSTRACT This review presents information on the relationship of ultrastructure and composition of wood cell walls, in order to understand how wood degrading bacteria utilise cell wall components for their nutrition. A brief outline of the structure and composition of plant cell walls and the degradation patterns associated with bacterial degradation of wood cell walls precedes the description of the relationship of cell wall micro- and ultrastructure to bacterial degradation of the cell wall. The main topics covered are cell wall structure and composition, patterns of cell wall degradation by erosion and tunnelling bacteria, and the relationship of cell wall ultrastructure and composition to wood degradation by erosion and tunnelling bacteria. Finally, pertinent information from select recent studies employing molecular approaches to identify bacteria which can degrade lignin and other wood cell wall components is presented, and prospects for future investigations on wood degrading bacteria are explored.
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Leclerc, Denis, and Alain Asselin. "Detection of bacterial cell wall hydrolases after denaturing polyacrylamide gel electrophoresis." Canadian Journal of Microbiology 35, no. 8 (August 1, 1989): 749–53. http://dx.doi.org/10.1139/m89-125.

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Cell walls from various Gram-positive bacteria were incorporated at a concentration of 0.2% (w/v) into polyacrylamide gels as a substrate for detection of cell wall hydrolases. Bacterial extracts from crude cell wall preparations were denatured with sodium dodecyl sulfate and 2-mercaptoethanol and subjected to denaturing polyacrylamide gel electrophoresis in gels containing bacterial cell walls. After renaturation in the presence of purified and buffered 1% (v/v) Triton X-100, cell wall hydrolases were visualized as clear lytic zones against the opaque cell wall background. One to fifteen bands with lytic activity could be detected, depending on bacterial extracts and on the nature of the cell walls incorporated into gels. Crude cell wall extracts were the best source of cell wall hydrolases from various Gram-positive bacteria such as Clostridium perfringens (15 bands), Micrococcus luteus (1 band), Bacillus megaterium (4 bands), Bacillus sp. (6 bands), B. cereus (3 bands), B. subtilis (7 bands), Staphylococcus aureus (13 bands), Streptococcus faecalis (3 bands), and Strep. pyogenes (5 bands). Molecular masses of cell wall hydrolases ranged from 17 to 114.6 kDa. Lytic activities against cell walls of Corynebacterium sepedonicum (Clavibacter michiganense pv. sepedonicum) could be shown with the cell wall extracts of Strep. pyogenes (45.7 kDa), Strep. faecalis (67 kDa), B. megaterium (67 kDa), and Staph. aureus (67 kDa).Key words: autolysins, electrophoresis, hydrolases, muramidases, peptidoglycan.
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Tokárová, Viola, Ayyappasamy Sudalaiyadum Perumal, Monalisha Nayak, Henry Shum, Ondřej Kašpar, Kavya Rajendran, Mahmood Mohammadi, et al. "Patterns of bacterial motility in microfluidics-confining environments." Proceedings of the National Academy of Sciences 118, no. 17 (April 19, 2021): e2013925118. http://dx.doi.org/10.1073/pnas.2013925118.

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Understanding the motility behavior of bacteria in confining microenvironments, in which they search for available physical space and move in response to stimuli, is important for environmental, food industry, and biomedical applications. We studied the motility of five bacterial species with various sizes and flagellar architectures (Vibrio natriegens, Magnetococcus marinus, Pseudomonas putida, Vibrio fischeri, and Escherichia coli) in microfluidic environments presenting various levels of confinement and geometrical complexity, in the absence of external flow and concentration gradients. When the confinement is moderate, such as in quasi-open spaces with only one limiting wall, and in wide channels, the motility behavior of bacteria with complex flagellar architectures approximately follows the hydrodynamics-based predictions developed for simple monotrichous bacteria. Specifically, V. natriegens and V. fischeri moved parallel to the wall and P. putida and E. coli presented a stable movement parallel to the wall but with incidental wall escape events, while M. marinus exhibited frequent flipping between wall accumulator and wall escaper regimes. Conversely, in tighter confining environments, the motility is governed by the steric interactions between bacteria and the surrounding walls. In mesoscale regions, where the impacts of hydrodynamics and steric interactions overlap, these mechanisms can either push bacteria in the same directions in linear channels, leading to smooth bacterial movement, or they could be oppositional (e.g., in mesoscale-sized meandered channels), leading to chaotic movement and subsequent bacterial trapping. The study provides a methodological template for the design of microfluidic devices for single-cell genomic screening, bacterial entrapment for diagnostics, or biocomputation.
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Singh, Adya P., Shruti Singh, and Ehsan Bari. "Bacterial Degradation of Wood by Tunnel Formation: Role of TEM in Understanding the Intricate Architecture of Tunnels and the Cell Wall Degradation Process." Microscopy Today 30, no. 5 (September 2022): 24–30. http://dx.doi.org/10.1017/s1551929522001080.

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Abstract:Certain bacteria degrade wood by creating tunnels in cell walls. Transmission electron microscopy (TEM) has played a key role in understanding the intricate architecture of the tunnels produced within the cell wall and the process of cell wall degradation. The most prominent feature of tunnels is the presence of periodic crescent-shaped slime bands, which is the single most important diagnostic characteristic of bacterial tunneling-type cell wall degradation. The review presented covers the aspects relevant to understanding bacterial tunneling of wood cell walls, emphasizing the importance of the application of TEM in this area of research.
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Kennedy, John F., and Jiro Shimizu. "Bacterial cell wall." Carbohydrate Polymers 29, no. 3 (March 1996): 294. http://dx.doi.org/10.1016/0144-8617(96)82557-4.

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Tsuneda, A., and R. G. Thorn. "Interactions of wood decay fungi with other microorganisms, with emphasis on the degradation of cell walls." Canadian Journal of Botany 73, S1 (December 31, 1995): 1325–33. http://dx.doi.org/10.1139/b95-394.

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Interactions of two wood decay fungi, Lentinula edodes and Pleurotus ostreatus, with other wood inhabiting microorganisms were investigated on agar and in fagaceous wood, primarily by scanning electron microscopy. Micromorphologically, there were two principal modes of cell wall degradation: (i) selective removal of amorphous wall components, followed by the degradation of skeletal microfibrils, and (ii) simultaneous degradation of all wall components. These two modes were observed in three different degradation systems: (i) sapwood wall degradation by the wood decay fungi, (ii) hyphal wall degradation by mycoparasitic Trichoderma, and (iii) hyphal wall degradation by pathogenic bacteria. The simultaneous-type wall degradation in the systems i and ii was usually caused by hyphal tips. In addition to the three systems, bacteriolysis by the wood decay fungi was also studied. The bacterial cell walls, as well as microfibril bundles of wood cellulose and fungal chitin, were all fragmented into minute granules at later stages of microbial degradation and the granules were further degraded into smaller units. Frequency of occurrence and strength of mycoparasitic activity of Trichoderma harzianum were influenced by the degree of wood decay where the interaction occurred. Presence of both cellulose and chitin microfibrils apparently enhanced the mycoparasitic activity. In Quercus wood, P. ostreatus showed a unidirectional growth toward bacterial colonies, which formed as the result of decomposition of dead nematodes, and consumed the unidentified bacteria. In nitrogen-deficient wood, fungal and bacterial cell walls may serve as an important reservoir of nitrogen for wood inhabiting microorganisms. Key words: wood decay, mycoparasitism, bacteriolysis, cellulose, chitin.
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Shan, Li, Qin Wenling, Panunzio Mauro, and Biondi Stefano. "Antibacterial Agents Targeting the Bacterial Cell Wall." Current Medicinal Chemistry 27, no. 17 (June 4, 2020): 2902–26. http://dx.doi.org/10.2174/0929867327666200128103653.

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The introduction of antibiotics to treat bacterial infections either by killing or blocking their growth has been accompanied by the studies of mechanism that allows the drugs to kill the bacteria or to stop their proliferation. In such a scenario, the emergence of antibacterial agents active on the bacterial cell wall has been of fundamental importance in the fight against bacterial agents responsible for severe diseases. As a matter of fact, the cell wall, which plays many roles during the lifecycle, is an essential constituent of most bacteria. This overview focuses on the intracellular steps of peptidoglycan biosynthesis and the research of new antibacterial agents based on the enzymes involved in these early steps of the formation of cell membrane components.
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Do, Truc, Julia E. Page, and Suzanne Walker. "Uncovering the activities, biological roles, and regulation of bacterial cell wall hydrolases and tailoring enzymes." Journal of Biological Chemistry 295, no. 10 (January 23, 2020): 3347–61. http://dx.doi.org/10.1074/jbc.rev119.010155.

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Bacteria account for 1000-fold more biomass than humans. They vary widely in shape and size. The morphological diversity of bacteria is due largely to the different peptidoglycan-based cell wall structures that encase bacterial cells. Although the basic structure of peptidoglycan is highly conserved, consisting of long glycan strands that are cross-linked by short peptide chains, the mature cell wall is chemically diverse. Peptidoglycan hydrolases and cell wall–tailoring enzymes that regulate glycan strand length, the degree of cross-linking, and the addition of other modifications to peptidoglycan are central in determining the final architecture of the bacterial cell wall. Historically, it has been difficult to biochemically characterize these enzymes that act on peptidoglycan because suitable peptidoglycan substrates were inaccessible. In this review, we discuss fundamental aspects of bacterial cell wall synthesis, describe the regulation and diverse biochemical and functional activities of peptidoglycan hydrolases, and highlight recently developed methods to make and label defined peptidoglycan substrates. We also review how access to these substrates has now enabled biochemical studies that deepen our understanding of how bacterial cell wall enzymes cooperate to build a mature cell wall. Such improved understanding is critical to the development of new antibiotics that disrupt cell wall biogenesis, a process essential to the survival of bacteria.
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Šimelyte, Egle, Marja Rimpiläinen, Leena Lehtonen, Xiang Zhang, and Paavo Toivanen. "Bacterial Cell Wall-Induced Arthritis: Chemical Composition and Tissue Distribution of Four Lactobacillus Strains." Infection and Immunity 68, no. 6 (June 1, 2000): 3535–40. http://dx.doi.org/10.1128/iai.68.6.3535-3540.2000.

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ABSTRACT To study what determines the arthritogenicity of bacterial cell walls, cell wall-induced arthritis in the rat was applied, using four strains of Lactobacillus. Three of the strains used proved to induce chronic arthritis in the rat; all were Lactobacillus casei. The cell wall of Lactobacillus fermentum did not induce chronic arthritis. All arthritogenic bacterial cell walls had the same peptidoglycan structure, whereas that of L. fermentum was different. Likewise, all arthritogenic cell walls were resistant to lysozyme degradation, whereas the L. fermentum cell wall was lysozyme sensitive. Muramic acid was observed in the liver, spleen, and lymph nodes in considerably larger amounts after injection of an arthritogenicL. casei cell wall than following injection of a nonarthritogenic L. fermentum cell wall. The L. casei cell wall also persisted in the tissues longer than theL. fermentum cell wall. The present results, taken together with those published previously, underline the possibility that the chemical structure of peptidoglycan is important in determining the arthritogenicity of the bacterial cell wall.
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Dissertations / Theses on the topic "Bacterial wall"

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Somner, Elizabeth Ann. "Antibiotic inhibitors of bacterial cell wall synthesis." Thesis, University of Cambridge, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.359831.

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Mattinson-Rose, A. D. "Classification of amycolate wall chemotype IV actinomycetes." Thesis, University of Newcastle Upon Tyne, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.374849.

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Bjertsjö, Rennermalm Anna. "Staphylococcal cell wall associated proteins : characteristics and host interactions /." Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-542-9/.

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Markovski, Monica. "Bacterial Cell Wall Synthases Require Outer Membrane Lipoprotein Cofactors." Thesis, Harvard University, 2012. http://dissertations.umi.com/gsas.harvard:10146.

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To fortify their cytoplasmic membrane and protect it from osmotic rupture, most bacteria surround themselves with a peptidoglycan (PG) exoskeleton. The PG synthases that build this structure are called penicillin-binding proteins (PBPs). Since they are the targets of penicillin and related antibiotics, the structures and in vitro biochemical functions of the PBPs have been extensively studied. However, the in vivo functions of the PBPs and the factors they work with to build the PG meshwork remain poorly understood. PBPs work in the context of multicomponent complexes organized by cytoskeletal elements. A major outstanding question has been whether or not these complexes contain factors required for PBP function. I addressed this using Escherichia coli as a model system by taking advantage of the synthetic lethal phenotype resulting from simultaneous inactivation of the major PG synthases: PBP1a and PBP1b. Using a screen for mutants synthetically lethal with the inactivation of PBP1b, I identified LpoA as a factor required for PBP1a function. A colleague in the lab performed the analogous screen for mutants synthetically lethal with the inactivation of PBP1a and identified LpoB as a factor required for PBP1b function. We showed that the Lpo factors are outer membrane lipoproteins that form specific trans-envelope complexes with their cognate PBPs in the inner membrane and that LpoB can stimulate the activity of PBP1b in vitro. Our results reveal unexpected complexity in the control of PBP activity and indicate that they likely receive regulatory input from the outer membrane in addition to cytoskeletal elements in the cytoplasm. To investigate the role of LpoB in morphogenesis further, I took a genetic approach that has identified PBP1b* variants capable of functioning in vivo in the absence of LpoB. Preliminary characterization of these variants indicates that LpoB has cellular functions in addition to PBP1b activation and that LpoB may be important for coordinating the two different catalytic activities of PBP1b. Future study of these mutants is likely to uncover important insights into PBP function and their control by the Lpo factors. These insights may open new avenues for the development of novel therapeutics that target the PBPs.
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Millward-Sadler, Sarah Jane. "The molecular biology of bacterial xylanases." Thesis, University of Newcastle Upon Tyne, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318256.

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Poole, Deborah Marie. "Molecular analysis of plant cell wall hydrolases of bacterial origin." Thesis, University of Newcastle Upon Tyne, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.238939.

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Choudhry, Anthony Ejaz. "Inhibition of bacterial cell wall biosynthesis by the affinity label N-bromoacetylglucosamine." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/MQ40403.pdf.

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Lancaster, M. J. "Studies on the export of extracellular proteins through the bacterial cell wall." Thesis, University of Bristol, 1985. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.356221.

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Reynolds, Catherine B. "A lesson in bacterial variability : the C. difficile cell wall protein CwpV." Thesis, Imperial College London, 2011. http://hdl.handle.net/10044/1/6993.

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Clostridium difficile is the main cause of antibiotic-associated diarrhea, leading to significant morbidity and mortality, and putting considerable economic pressure on healthcare systems. Current knowledge of the molecular basis of pathogenesis is limited primarily to the activities and regulation of two major toxins. In contrast, little is known of the mechanisms used to colonise the enteric system. C. difficile expresses a proteinaceous array on its cell surface known as the S-layer, consisting primarily of SlpA and a family of homologues, the cell wall protein (CWP) family. CwpV is the largest member of this family. CwpV is expressed in a phase-variable manner controlled by an invertible DNA switch, the cwpV switch. The novel mechanism controlling this phase variation has been charaterised using enzymatic reporter assays. A site-specific recombinase (RecV) catalyzing the inversion of the cwpV switch has been identified. Knocking out this recombinase has enabled isolation of cwpV switch locked ON and locked OFF strains of C. difficile, indicating that cwpV switch orientation is the primary determinant of CwpV expression. CwpV is post-translationally cleaved and expressed on the cell surface as two proteins that form a stable complex, with one subunit responsible for the noncovalent cell wall anchoring of the other large repetitive subunit. Due to the significant heterogeneity of C. difficile strains the characteristics of CwpV across a panel of strains were investigated. The cwpV switch and recV are conserved across diverse strains and all strains tested express CwpV in a phase variable manner. The N-terminus of CwpV is well conserved, however the C-terminal repetitive domain of CwpV varies markedly. Five different types have been identified and shown to be antigenically distinct. All types of CwpV repeats promote aggregation of C. difficile cells, which may be an important function during infection. These findings suggest a complex evolutionary history for CwpV.
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Rayner, Joanna Clare. "The role of the bacterial cell wall in biofilm formation and antibiotic susceptibility." Thesis, University of Exeter, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.388624.

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Books on the topic "Bacterial wall"

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M, Ghuysen J., and Hackenbeck R. 1948-, eds. Bacterial cell wall. Amsterdam: Elsevier, 1994.

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Hong, Hee-Jeon, ed. Bacterial Cell Wall Homeostasis. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4939-3676-2.

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Seltmann, Guntram, and Otto Holst. The Bacterial Cell Wall. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-04878-8.

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Ton-That, Hung, ed. The Bacterial Cell Wall. New York, NY: Springer US, 2024. http://dx.doi.org/10.1007/978-1-0716-3491-2.

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S, Stewart-Tull D. E., and Davies M. 1932-, eds. Immunology of the bacterial cell envelope. Chichester: Wiley, 1985.

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1935-, Tipper Donald J., ed. Antibiotic inhibitorsof bacterial cell wall biosynthesis. Oxford: Pergamon, 1987.

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Cell wall deficient forms: Stealth pathogens. 3rd ed. Boca Raton, Fla: CRC Press, 2001.

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Cell wall deficient forms: Stealth pathogens. 2nd ed. Boca Raton, Fla: CRC Press, 1993.

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1935-, Tipper Donald J., ed. Antibiotic inhibitors of bacterial cell wall biosynthesis. Oxford [Oxfordshire]: Pergamon Press, 1987.

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König, Helmut. Prokaryotic Cell Wall Compounds: Structure and Biochemistry. Berlin, Heidelberg: Springer-Verlag Berlin Heidelberg, 2010.

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Book chapters on the topic "Bacterial wall"

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Chapot-Chartier, Marie-Pierre. "Bacterial Autolysins." In Prokaryotic Cell Wall Compounds, 383–406. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-05062-6_13.

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Corbett, David, Thomas Hudson, and Ian S. Roberts. "Bacterial Polysaccharide Capsules." In Prokaryotic Cell Wall Compounds, 111–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-05062-6_3.

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Seltmann, Guntram, and Otto Holst. "Cell Wall Models." In The Bacterial Cell Wall, 204–18. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-04878-8_7.

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Seltmann, Guntram, and Otto Holst. "Cell Wall Functions." In The Bacterial Cell Wall, 219–65. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-04878-8_8.

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Ginsberg, Cynthia, Stephanie Brown, and Suzanne Walker. "Bacterial Cell Wall Components." In Glycoscience, 1535–600. Berlin, Heidelberg: Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-30429-6_38.

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Baddiley, James. "Bacterial Cell Wall Biosynthesis." In Ciba Foundation Symposium 7 - Polymerization in Biological Systems, 87–107. Chichester, UK: John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470719909.ch6.

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Seltmann, Guntram, and Otto Holst. "Introduction." In The Bacterial Cell Wall, 3–8. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-04878-8_1.

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Seltmann, Guntram, and Otto Holst. "The Outer Membrane of the Gram-Negative Bacteria and their Components." In The Bacterial Cell Wall, 9–102. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-04878-8_2.

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Seltmann, Guntram, and Otto Holst. "Periplasmic Space and Rigid Layer." In The Bacterial Cell Wall, 103–32. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-04878-8_3.

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Seltmann, Guntram, and Otto Holst. "Further Cell Wall Components of Gram-Positive Bacteria." In The Bacterial Cell Wall, 133–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 2002. http://dx.doi.org/10.1007/978-3-662-04878-8_4.

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Conference papers on the topic "Bacterial wall"

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Zhu, L., M. Salloum, S. Feteih, J. Hough, D. Arola, and M. Tolba. "Experimental Study of Temperature Elevations in Extracted Teeth Using a System B Heating Catheter for Bacterial Disinfection." In ASME 2010 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2010. http://dx.doi.org/10.1115/sbc2010-19125.

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Total bacterial disinfection and elimination from the human root canal system are crucial in clinical endodontic procedures [Card et al., 2002; Kakoli et al., 2009]. The current approaches relying on mechanical instrumentation and root canal irrigation and medicaments have demonstrated that eradication of bacteria occurs when the bacteria are in direct contact with the medicaments. However, persistent infection following routine treatments has suggested that bacteria may harbor in the root canal anatomical irregularities and/or deep dentinal tubules, therefore, surface irrigation of medicaments may not be able to reach those regions. Heat treatment has been used for obturation of the root canal in endodontic practice. In this study we hypothesize that as an alternative, surface heating using a System B heating catheter through the root canal surface would be effective for bacterial elimination in the deep dentin. The heat-induced cytotoxic response kills bacteria in the root dentin via heat conduction from the thermal energy incident on the root canal wall. In principle, a high power setting and/or a long heating duration can always achieve sufficient temperature elevations in deep dentin. Yet, the detailed temperature distribution inside the dentin and possible thermal damage to the supporting periodontium are unknown. Therefore, it is of clinical importance to perform and investigate temperature elevations in dentin to provide clinicians with an optimized and effective treatment protocol to minimize unnecessary thermal damage to the surrounding structure.
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Even-Tzur, Nurit, Uri Zaretsky, Michael Wolf, and David Elad. "Respose of Cultured Nasal Epithelial Cells to Wall Shear Stress." In ASME 2007 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2007. http://dx.doi.org/10.1115/sbc2007-176374.

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The nasal cavity lining is rich with mucus secreting goblet cells. Nasal defense is based on the mucociliary clearance mechanism, in which the secreted mucus layer traps inhaled particles and is constantly driven towards the nasopharynx for removal of the particles from the body. The mucus layer is also important for the exchange of temperature and water vapor with the inspired air. Airway goblet cells discharge mucus in response to a wide variety of biological stimuli, including cytokines, bacterial products, proteinases, oxidants, irritant gases, and inflammatory mediators [1], as well as biophysical changes, such as osmolarity alterations [2].
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Pratama, Mohammad, and Isna Aziz. "Molecular Docking of Bawang Dayak (Eleutherine bulbosa) Secondary Metabolites as Bacterial Cell Wall Synthesis Inhibitor." In 1st International Conference on Science and Technology, ICOST 2019, 2-3 May, Makassar, Indonesia. EAI, 2019. http://dx.doi.org/10.4108/eai.2-5-2019.2284686.

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Alomari, Anaam. "High Resolution Imaging and Nanomechanical Properties of Gram-Positive Bacterial Cell Wall Using Atomic Force Microscopy." In Microscience Microscopy Congress 2021 incorporating EMAG 2021. Royal Microscopical Society, 2021. http://dx.doi.org/10.22443/rms.mmc2021.277.

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Mielnik, Michal M., and Lars R. Sætran. "Micro-PIV Investigation of a Sinusoidal Crossflow Microfiltration Module." In ASME 2003 1st International Conference on Microchannels and Minichannels. ASMEDC, 2003. http://dx.doi.org/10.1115/icmm2003-1118.

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A micro-PIV system is presented in detail, pointing out important aspects of micro-PIV system design cruicial for its operation. The micro-PIV system is then applied on a sinusoidal microchannel, and the fluid motion inside the device is presented and discussed. The wall shear stress at the waist of the channel is measured to be up to 60% higher than the wall shear stress in a conventional parallel-plate flow. The results suggest that altering of channel geometry may contribute to better design of cross-flow microfiltration units, in terms of reduced clogging by shear-control of bacterial motion. Furthermore, the flow is shown to exhibit a strong Reynolds number dependence, characterised by the onset of periodic distortion imposed on the flow by the sinusoidal walls occuring between Re = 2 and Re = 10.
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Salek, M., and R. J. Martinuzzi. "Numerical Simulation of Fluid Flow and Oxygen Transport in the Tube Flow Cells Containing Biofilms." In ASME/JSME 2007 5th Joint Fluids Engineering Conference. ASMEDC, 2007. http://dx.doi.org/10.1115/fedsm2007-37063.

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The hydrodynamics in flow systems is known to induce phenotypic changes associated with bacterial biofilms, including increased tolerance to antimicrobial agents and biocides. Results obtained in flow cells commonly used in biological and medical studies on the influence of flow on biofilm behavior and antimicrobial susceptibility are sometimes contradictory. It is thus hypothesized that discrepancies in the results may be related to the flow cell geometry. In this study, the shear stress distribution and substrate concentration were numerically simulated inside long rectangular and square tubes. The fluid was Newtonian and a uniform distribution of biofilms, which consume the substrate from the medium, was assumed on the walls. The consumption of oxygen by biofilms was assumed to follow the Monod kinetics. The effects of flow velocity, flow cell geometry, and substrate diffusivity on wall shear stress and substrate concentration distributions were investigated. Based on simulation results, differences observed in the morphology and response of biofilms can be directly related to hydrodynamic changes caused by the flow cell configuration.
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Libby, Peter, Stephen J. C. Warner, and Louis K. Birinyi. "THE VESSEL WALL AS A SOURCE OF VASORHGOLATORY AND IMMDNOSTIMOLATORY CYTOKINES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643982.

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The cytokines Interleukin-1 (IL-1) and Tumor Necrosis Factor (TNF, also known as cachectin) exhibit multiple effects on circulating blood cells and cells of the blood vessel wall. For example, these mediators elicit a coordinated Drogram of functions of endothelial cells (EC) that promotes blood coagulation and thrombosis, and lead to clot stabilization. Furthermore, IL-1 and TNF promote adherence to vascular endothelium of leukocytes of many classes.Thus, these cytokines are likely to be involved in signaling the pathologic changes in blood vessels that characterize a number of inflammatory or infectious processes. These two cytokines were originally isolated frcm activated human mononuclear phagocytes, hence their comnon designation as monokines and the terminology "interleukin". However, recent findings have broadened this concept considerably. It is now clear that many cell types can produce IL-1-1ike activity.Several groups showed that human vascular EC can secrete material that stimulates proliferation of thymocytes incubated with suboptima1 doses of the mitogenic lectin phytohemagglutinin, a typical acitivty of IL-1 (thymocyte costimulation).Two related but distinct genes cloned frcm human peripheral blood monocytes encode IL-1 molecules. In human blood monocytes stimulated with bacterial lioopolysaccharide (LPS) IL-1 beta (pi ∼ 7) is the major form expressed while IL-1 alpha (pi ∼ 5) is the less abundant species secreted by human monocytes under these conditions. We found that EC and smooth muscle cells (SMC) isolated from adult human vessels can express these same IL-1 genes. LPS, a standard stimulus to IL-1 secretion in the monocyte, caused accumulation of IL-1 beta mRNA in both vascular cell types. Endothelial cells frcm adult human vessels also contained IL-1 alpha mRNA when treated with LPS in the presence of cycloheximide and LPS-stimulated smooth muscle cells contained RNA that hybridized with an IL-1 alpha cDNA probe as well. Although both vascular cell types can transcribe these IL-1 genes, the time course of this response differs. LPS induced IL-1 beta mRNA production by SMC maximally at 4-6 hr., whereas maximal IL-1 induction by LPS in EC occured 1 day after initiation of the exposure. Actinanycin D (1 ug/ml) blocked 3H-uridine incorporation into macromolecules by > 95% in both EC & SMC, and prevented the LPS-induced increases in IL-1 mRNA levels in these cells. This result suggests that this potentially injurious stimulus causes IL-1 mRNA accumulation by an increase in rates of transcription. These LPS-induced increases in IL-1 mRNA levels corresponded to production of biologically active IL-1 determined as thymocyte costimulation activity. Interestingly, gel filtration experiments revealed a molecular weight of around 22kD for both SMC and EC-derived IL-1 secreted into culture medium in response to LPS. This molecular weight contrasts with the 17 kD species which is the fully processed product secreted frcm activated human monocytes. A possible explanation for this disparity is that the vascular cells secrete a partially processed intermediate form of mature IL-1. Other stimuli for IL-1 mRNA accumulation and secretion of biological activity include TNF and IL-1 itself. Recombinant human INF (≥ 10 ng/ml) increased IL-1 beta mRNA levels in EC & SMC, and caused the EC & SMC to release IL-1-1 ike thymocyte costimulation activity. Of interest is the recent observation that IL-1 itself can stimulate expression of IL-rl genes in vascular wall cells. Both IL-1 aloha and beta can increase IL-1 beta mRNA content in EC & SMC. Hris observation was confirmed with homogenous IL-1 prepared by recombinant DNA technologies (rIL-1). These findings raise the possibility of a novel positive feedback loop in vascular pathophysiology. We also found that rIL-1 alpha or beta also induced the production of prostaglandin E2 (PGE2) by both vascular SMC & EC. This prostanoid, induced by IL-1, inhibits thymocyte _ proliferation. Thus, IL-1 not only induced its own expression but increased production of this immunosuppressive prostanoid. This mechanism provides a potential negative control loop in regulation of the local immune response in blood vessels. Vie conclude that these cells of the blood vessel wall are a source of the potent vasoregulatory and immune mediators IL-1 alpha and beta. Since IL-1 influences the thrombotic, hemostatic, and fibrinolytic functions of endothelium, as well as other responses to acute injury, our findings suggest novel local control mechanisms that may be important in a variety of pathologic states.
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Vladu, Alina, Emilia Visileanu, Alina Popescu, and Roxana Rodica Constantinescu. "Antimicrobial treatments of undergarments designed for the combat-protective clothing of soldiers." In AHFE 2023 Hawaii Edition. AHFE International, 2023. http://dx.doi.org/10.54941/ahfe1004210.

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Military forces around the world must be equipped with combat-protective clothing made from the best technical textiles available that must provide sufficient protection, increased comfort, and even antimicrobial protection, especially for underwear pieces. Antibacterial treatments for textile materials include the use of various substances such as chitosan, silver, collagen and so on. Chitosan is a polysaccharide that promotes changes in the permeability properties of the membrane wall causing internal osmotic imbalances and consequently inhibits the growth of microorganisms. Silver can also damage the bacterial RNA and DNA, eventually leading to the bacteria`s death. Moreover, collagen, a fibrous natural protein, has an intrinsic ability to fight infection and contributes to keeping the infection site sterile.This paper focuses on the functionalization of four variants of textile materials with different compositions to increase their antibacterial properties. The variants were treated through two different technologies: exhaustion (30 min at 40°C, 500 rpm) and padding (3 consecutive passes). V1-V4 were functionalized with colloidal silver and V1-V3 with a mixture of collagen hydrolysate and colloidal silver through exhaustion. Variants V1-V3 were also treated through the padding technique using 0.5% chitosan, 1% collagen hydrolysate and a mixture of chitosan and colloidal silver. Untreated textile variants were evaluated regarding their physical-mechanical characteristics. Moreover, the functionalized variants were characterised according to their pH, loading degree with active substances (%), wettability by drop test and contact angle methods, thermal resistance (m2K/W) and vapour resistance (m2Pa/W) according to ISO 11092. Treated textile samples were also investigated relating to their antimicrobial resistance using two methods according to ISO 20743/2013 and SR EN ISO 20645/2005. The evaluation of antibacterial resistance using the standards SR EN ISO 20645/2005 and SR EN ISO 20645/2005 demonstrated the effectiveness of treatments with active substances for approx. 95% of the tested variants.
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Zheng, Zhouyuan, Parth Bansal, and Yumeng Li. "Numerical Study on Antibacterial Effects of Bio-Inspired Nanostructured Surface." In ASME 2020 International Mechanical Engineering Congress and Exposition. American Society of Mechanical Engineers, 2020. http://dx.doi.org/10.1115/imece2020-23594.

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Abstract Natural bactericidal surfaces are found on the wings of cicada and dragonfly that compose of nanopatterns such as nanopillar arrays. Experimental studies have unveiled that the nanopillars can penetrate the bacterial walls or stretch them, resulting in the cell death. This offers an attractive “chemical-free” and wide-spectrum strategy to fight against bacteria-related infections and fouling, especially for implant-associated infections (IAIs). However, what is the fundamental mechanism and key factors governing the bactericidal performance of the nanostructured surface is the critical research questions need to be answered to realize its full potential. In this work, we developed mechanical single cell model of bacteria based on finite element analysis (FEA) to simulate the interactions between different strains of bacteria and the nanostructured surface. The nanostructured surface contains nanopillar arrays, which are made of polymer materials. Different strains of bacteria are simulated by adopting the corresponding geometry and material properties from experimental values. The mechanical responses of the bacteria cell on the nanopillar arrays with various configurations are studied based on estimated stress and strain distributions within the cell.
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Wong, Denise, Edward B. Steager, and Vijay Kumar. "Near-Wall Dynamics and Photoresponse of Swimming Microbiorobots." In ASME 2012 International Design Engineering Technical Conferences and Computers and Information in Engineering Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/detc2012-71033.

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At the microscale, the ability to precisely move objects on the scale of microns is a challenge. One method is to use microbiorobots (MBRs), constructed of a neutrally-buoyant microstructure powered by a monolayer of swarmer flagellated bacteria adhered to the surface. The bacteria swim to propel the microstructure in a fluidic environment in the absence of external forces. The trajectory is a combination of translation and rotation, with the rotation generally observed to be clockwise when viewed from above. In order to create a dynamic model of the inherent motion of MBRs, we use UV light to immobilize the bacteria on different regions of an MBR and characterize the resultant motion. We show that the bacteria on the edge of the structure have different force contributions than those in the center of the microstructure where the flagella cannot interact with the surface under that MBR. This is a step towards improved accuracy in the control of MBRs when external forces are applied for manipulation.
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Reports on the topic "Bacterial wall"

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Manulis, Shulamit, Christine D. Smart, Isaac Barash, Guido Sessa, and Harvey C. Hoch. Molecular Interactions of Clavibacter michiganensis subsp. michiganensis with Tomato. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7697113.bard.

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Clavibacter michiganensis subsp. michiganensis (Cmm), the causal agent of bacterial wilt and canker of tomato, is the most destructive bacterial disease of tomato causing substantial economic losses in Israel, the U.S.A. and worldwide. The molecular strategies that allow Cmm, a Gram-positive bacterium, to develop a successful infection in tomato plants are largely unknown. The goal of the project was to elucidate the molecular interactions between Cmmand tomato. The first objective was to analyze gene expression profiles of susceptible tomato plants infected with pathogenic and endophytic Cmmstrains. Microarray analysis identified 122 genes that were differentially expressed during early stages of infection. Cmm activated typical basal defense responses in the host including induction of defense-related genes, production of scavenging of free oxygen radicals, enhanced protein turnover and hormone synthesis. Proteomic investigation of the Cmm-tomato interaction was performed with Multi-Dimensional Protein Identification Technology (MudPIT) and mass spectroscopy. A wide range of enzymes secreted by Cmm382, including cell-wall degrading enzymes and a large group of serine proteases from different families were identified in the xylem sap of infected tomato. Based on proteomic results, the expression pattern of selected bacterial virulence genes and plant defense genes were examined by qRT-PCR. Expression of the plasmid-borne cellulase (celA), serine protease (pat-1) and serine proteases residing on the chp/tomA pathogenicity island (chpCandppaA), were significantly induced within 96 hr after inoculation. Transcription of chromosomal genes involved in cell wall degradation (i.e., pelA1, celB, xysA and xysB) was also induced in early infection stages. The second objective was to identify by VIGS technology host genes affecting Cmm multiplication and appearance of disease symptoms in plant. VIGS screening showed that out of 160 tomato genes, which could be involved in defense-related signaling, suppression of 14 genes led to increase host susceptibility. Noteworthy are the genes Snakin-2 (inhibitor of Cmm growth) and extensin-like protein (ELP) involved in cell wall fortification. To further test the significance of Snakin -2 and ELP in resistance towards Cmm, transgenic tomato plants over-expressing the two genes were generated. These plants showed partial resistance to Cmm resulting in a significant delay of the wilt symptoms and reduction in size of canker lesion compared to control. Furthermore, colonization of the transgenic plants was significantly lower. The third objective was to assess the involvement of ethylene (ET), jasmonate (JA) and salicylic acid (SA) in Cmm infection. Microarray and proteomic studies showed the induction of enzymes involved in ET and JA biosynthesis. Cmm promoted ET production 8 days after inoculation and SIACO, a key enzyme of ET biosynthesis, was upregulated. Inoculation of the tomato mutants Never ripe (Nr) impaired in ET perception and transgenic plants with reduced ET synthesis significantly delayed wilt symptoms as compared to the wild-type plants. The retarded wilting in Nr plants was shown to be a specific effect of ET insensitivity and was not due to altered expression of defense related genes, reduced bacterial population or decrease in ethylene biosynthesis . In contrast, infection of various tomato mutants impaired in JA biosynthesis (e.g., def1, acx1) and JA insensitive mutant (jai1) yielded unequivocal results. The fourth objective was to determine the role of cell wall degrading enzymes produced by Cmm in xylem colonization and symptoms development. A significance increase (2 to 7 fold) in expression of cellulases (CelA, CelB), pectate lyases (PelA1, PelA2), polygalacturonase and xylanases (XylA, XylB) was detected by qRT-PCR and by proteomic analysis of the xylem sap. However, with the exception of CelA, whose inactivation led to reduced wilt symptoms, inactivation of any of the other cell wall degrading enzymes did not lead to reduced virulence. Results achieved emphasized the complexity involved in Cmm-tomato interactions. Nevertheless they provide the basis for additional research which will unravel the mechanism of Cmm pathogenicity and formulating disease control measures.
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Manulis-Sasson, Shulamit, Christine D. Smart, Isaac Barash, Laura Chalupowicz, Guido Sessa, and Thomas J. Burr. Clavibacter michiganensis subsp. michiganensis-tomato interactions: expression and function of virulence factors, plant defense responses and pathogen movement. United States Department of Agriculture, February 2015. http://dx.doi.org/10.32747/2015.7594405.bard.

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Clavibactermichiganensissubsp. michiganensis(Cmm), the causal agent of bacterial wilt and canker of tomato, is the most destructive bacterial disease of tomato causing substantial economic losses in Israel, the U.S.A. and worldwide. The goal of the project was to unravel the molecular strategies that allow Cmm, a Gram-positive bacterium, to develop a successful infection in tomato. The genome of Cmm contains numerous genes encoding for extracellular serine proteases and cell wall degrading enzymes. The first objective was to elucidate the role of secreted serine proteases in Cmm virulence. Mutants of nine genes encoding serine proteases of 3 different families were tested for their ability to induce wilting, when tomato stems were puncture-inoculated, as compared to blisters formation on leaves, when plants were spray-inoculated. All the mutants showed reduction in wilting and blister formation as compared to the wild type. The chpCmutant displayed the highest reduction, implicating its major role in symptom development. Five mutants of cell wall degrading enzymes and additional genes (i.e. perforin and sortase) caused wilting but were impaired in their ability to form blisters on leaves. These results suggest that Cmm differentially expressed virulence genes according to the site of penetration. Furthermore, we isolated and characterized two Cmmtranscriptional activators, Vatr1 and Vatr2 that regulate the expression of virulence factors, membrane and secreted proteins. The second objective was to determine the effect of bacterial virulence genes on movement of Cmm in tomato plants and identify the routes by which the pathogen contaminates seeds. Using a GFP-labeledCmm we could demonstrate that Cmm extensively colonizes the lumen of xylem vessels and preferentially attaches to spiral secondary wall thickening of the protoxylem and formed biofilm-like structures composed of large bacterial aggregates. Our findings suggest that virulence factors located on the chp/tomAPAI or the plasmids are required for effective movement of the pathogen in tomato and for the formation of cellular aggregates. We constructed a transposon plasmid that can be stably integrated into Cmm chromosome and express GFP, in order to follow movement to the seeds. Field strains from New York that were stably transformed with this construct, could not only access seeds systemically through the xylem, but also externally through tomato fruit lesions, which harbored high intra-and intercellular populations. Active movement and expansion of bacteria into the fruit mesocarp and nearby xylem vessels followed, once the fruit began to ripen. These results highlight the ability of Cmm to invade tomato fruit and seed through multiple entry routes. The third objective was to assess correlation between disease severity and expression levels of Cmm virulence genes and tomato defense genes. The effect of plant age on expression of tomato defense related proteins during Cmm infection was analyzed by qRT-PCR. Five genes out of eleven showed high induction at early stages of infection of plants with 19/20 leaves compared to young plants bearing 7/8 leaves. Previous results showed that Cmm virulence genes were expressed at early stages of infection in young plants compared to older plants. Results of this study suggest that Cmm virulence genes may suppress expression of tomato defense-related genes in young plants allowing effective disease development. The possibility that chpCis involved in suppression of tomato defense genes is currently under investigation by measuring the transcript level of several PR proteins, detected previously in our proteomics study. The fourth objective was to define genome location and stability of virulence genes in Cmm strains. New York isolates were compared to Israeli, Serbian, and NCPPB382 strains. The plasmid profiles of New York isolates were diverse and differed from both Israeli and Serbian strains. PCR analysis indicated that the presence of putative pathogenicity genes varied between isolates and highlighted the ephemeral nature of pathogenicity genes in field populations of Cmm. Results of this project significantly contributed to the understanding of Cmm virulence, its movement within tomato xylem or externally into the seeds, the role of serine proteases in disease development and initiated research on global regulation of Cmm virulence. These results form a basis for developing new strategies to combat wilt and canker disease of tomato.
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Harman, Gary E., and Ilan Chet. Discovery and Use of Genes and Gene Combinations Coding for Proteins Useful in Biological Control. United States Department of Agriculture, September 1994. http://dx.doi.org/10.32747/1994.7568787.bard.

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The objectives of the research in this proposal were to (A) identify synergy among proteins that provide enhanced activity over single proteins for control of plant pathogenic fungi, (B) clone and characterize genetic sequences coding for proteins with ability to control pathogenic fungi, (C) produce transgenic organisms with enhanced biocontrol ability using genes and gene combinations and determine their efficiency in protecting plants against plant pathogenic fungi. A related objective was to produce disease-resistant plants. Fungal cell wall degrading enzymes from any source are strongly synergistic with any membrane active compound and, further, different classes of cell wall degrading enzymes are also strongly synergistic. We have cloned and sequenced a number of genes from bacterial and fungal sources including five that are structurally unrelated. We have prepared transgenic fungi that are deficient in production of enzymes and useful in mechanistic studies. Others are hyperproducers of specific enzymes that permit us, for the first time, to produce enzymes from T. harzianum in sufficient quantity to conduct tests of their potential use in commercial agriculture. Finally, genes from these studies have been inserted into several species of crop plants were they produce a high level of resistance to several plant pathogenic fungi.
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Sessa, Guido, and Gregory Martin. MAP kinase cascades activated by SlMAPKKKε and their involvement in tomato resistance to bacterial pathogens. United States Department of Agriculture, January 2012. http://dx.doi.org/10.32747/2012.7699834.bard.

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The research problem: Pseudomonas syringae pv. tomato (Pst) and Xanthomonas campestrispv. vesicatoria (Xcv) are the causal agents of tomato bacterial speck and spot diseases, respectively. These pathogens colonize the aerial parts of the plant and cause economically important losses to tomato yield worldwide. Control of speck and spot diseases by cultural practices or chemicals is not effective and genetic sources of resistance are very limited. In previous research supported by BARD, by gene expression profiling we identified signaling components involved in resistance to Xcvstrains. Follow up experiments revealed that a tomato gene encoding a MAP kinase kinase kinase (MAPKKKe) is required for resistance to Xcvand Pststrains. Goals: Central goal of this research was to investigate the molecular mechanisms by which MAPKKKεand associated MAP kinase cascades regulate host resistance. Specific objectives were to: 1. Determine whether MAPKKKεplays a broad role in defense signaling in plants; 2. Identify components of MAP kinase cascades acting downstream of MAPKKKε; 3. Determine the role of phosphorylation-related events in the function of MAPKKKε; 4. Isolate proteins directly activated by MAPKKKε-associatedMAPK modules. Our main achievements during this research program are in the following major areas: 1. Characterization of MAPKKKεas a positive regulator of cell death and dissection of downstream MAP kinase cascades (Melech-Bonfil et al., 2010; Melech-Bonfil and Sessa, 2011). The MAPKKKεgene was found to be required for tomato resistance to Xcvand Pstbacterial strains and for hypersensitive response cell death triggered by different R gene/effector gene pairs. In addition, overexpression analysis demonstrated that MAPKKKεis a positive regulator of cell death, whose activity depends on an intact kinase catalytic domain. Epistatic experiments delineated a signaling cascade downstream of MAPKKKεand identified SIPKK as a negative regulator of MAPKKKε-mediated cell death. Finally, genes encoding MAP kinase components downstream of MAPKKKεwere shown to contribute to tomato resistance to Xcv. 2. Identification of tomato proteins that interact with MAPKKKεand play a role in plant immunity (Oh et al., 2011). We identified proteins that interact with MAPKKKε. Among them, the 14-3-3 protein TFT7 was required for cell death mediated by several R proteins. In addition, TFT7 interacted with the MAPKK SlMKK2 and formed homodimersin vivo. Thus, TFT7 is proposed to recruit SlMKK2 and MAPKKK client proteins for efficient signal transfer. 3. Development of a chemical genetic approach to identify substrates of MAPKKKε-activated MAP kinase cascades (Salomon et al., 2009, 2011). This approach is based on engineering the kinase of interest to accept unnatural ATP analogs. For its implementation to identify substrates of MAPKKKε-activated MAP kinase modules, we sensitized the tomato MAP kinase SlMPK3 to ATP analogs and verified its ability to use them as phosphodonors. By using the sensitized SlMPK3 and radiolabeled N6(benzyl)ATP it should be possible to tag direct substrates of this kinase. 4. Development of methods to study immunity triggered by pathogen-associated molecular patterns (PAMPs) in tomato and N. benthamiana plants (Kim et al., 2009; Nguyen et al. 2010). We developed protocols for measuring various PTI-associatedphenotypes, including bacterial populations after pretreatment of leaves with PAMPs, induction of reporter genes, callose deposition at the cell wall, activation of MAP kinases, and a luciferase-based reporter system for use in protoplasts. Scientific and agricultural significance: Our research activities discovered and characterized a signal transduction pathway mediating plant immunity to bacterial pathogens. Increased understanding of molecular mechanisms of immunity will allow them to be manipulated by both molecular breeding and genetic engineering to produce plants with enhanced natural defense against disease. In addition, we successfully developed new biochemical and molecular methods that can be implemented in the study of plant immunity and other aspects of plant biology.
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Splitter, Gary A., Menachem Banai, and Jerome S. Harms. Brucella second messenger coordinates stages of infection. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7699864.bard.

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Aim 1: To determine levels of this second messenger in: a) B. melitensiscyclic-dimericguanosinemonophosphate-regulating mutants (BMEI1448, BMEI1453, and BMEI1520), and b) B. melitensis16M (wild type) and mutant infections of macrophages and immune competent mice. (US lab primary) Aim 2: To determine proteomic differences between Brucelladeletion mutants BMEI1453 (high cyclic-dimericguanosinemonophosphate, chronic persistent state) and BMEI1520 (low cyclicdimericguanosinemonophosphate, acute virulent state) compared to wild type B. melitensisto identify the role of this second messenger in establishing the two polar states of brucellosis. (US lab primary with synergistic assistance from the Israel lab Aim 3: Determine the level of Brucellacyclic-dimericguanosinemonophosphate and transcriptional expression from naturally infected placenta. (Israel lab primary with synergistic assistance from the US lab). B. Background Brucellaspecies are Gram-negative, facultative intracellular bacterial pathogens that cause brucellosis, the most prevalent zoonosis worldwide. Brucellosis is characterized by increased abortion, weak offspring, and decreased milk production in animals. Humans are infected with Brucellaby consuming contaminated milk products or via inhalation of aerosolized bacteria from occupational hazards. Chronic human infections can result in complications such as liver damage, orchitis, endocarditis, and arthritis. Brucellaspp. have the ability to infect both professional and non-professional phagocytes. Because of this, Brucellaencounter varied environments both throughout the body and within a cell and must adapt accordingly. To date, few virulence factors have been identified in B. melitensisand even less is known about how these virulence factors are regulated. Subsequently, little is known about how Brucellaadapt to its rapidly changing environments, and how it alternates between acute and chronic virulence. Our studies suggest that decreased concentrations of cyclic dimericguanosinemonophosphate (c-di-GMP) lead to an acute virulent state and increased concentrations of c-di-GMP lead to persistent, chronic state of B. melitensisin a mouse model of infection. We hypothesize that B. melitensisuses c-di-GMP to transition from the chronic state of an infected host to the acute, virulent stage of infection in the placenta where the bacteria prepare to infect a new host. Studies on environmental pathogens such as Vibrio choleraeand Pseudomonas aeruginosasupport a mechanism where changes in c-di-GMP levels cause the bacterium to alternate between virulent and chronic states. Little work exists on understanding the role of c-di-GMP in dangerous intracellular pathogens, like Brucellathat is a frequent pathogen in Israeli domestic animals and U.S. elk and bison. Brucellamust carefully regulate virulence factors during infection of a host to ensure proper expression at appropriate times in response to host cues. Recently, the novel secondary signaling molecule c-di-GMP has been identified as a major component of bacterial regulation and we have identified c-di-GMP as an important signaling factor in B. melitensishost adaptation. C. Major conclusions, solutions, achievements 1. The B. melitensis1453 deletion mutant has increased c-di-GMP, while the 1520 deletion mutant has decreased c-di-GMP. 2. Both mutants grow similarly in in vitro cultures; however, the 1453 mutant has a microcolony phenotype both in vitro and in vivo 3. The 1453 mutant has increased crystal violet staining suggesting biofilm formation. 4. Scanning electron microscopy revealed an abnormal coccus appearance with in increased cell area. 5. Proteomic analysis revealed the 1453 mutant possessed increased production of proteins involved in cell wall processes, cell division, and the Type IV secretion system, and a decrease in proteins involved in amino acid transport/metabolism, carbohydrate metabolism, fatty acid production, and iron acquisition suggesting less preparedness for intracellular survival. 6. RNAseq analysis of bone marrow derived macrophages infected with the mutants revealed the host immune response is greatly reduced with the 1453 mutant infection. These findings support that microlocalization of proteins involved in c-di-GMP homeostasis serve a second messenger to B. melitensisregulating functions of the bacteria during infection of the host.
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Morrison, Mark, Joshuah Miron, Edward A. Bayer, and Raphael Lamed. Molecular Analysis of Cellulosome Organization in Ruminococcus Albus and Fibrobacter Intestinalis for Optimization of Fiber Digestibility in Ruminants. United States Department of Agriculture, March 2004. http://dx.doi.org/10.32747/2004.7586475.bard.

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Improving plant cell wall (fiber) degradation remains one of the highest priority research goals for all ruminant enterprises dependent on forages, hay, silage, or other fibrous byproducts as energy sources, because it governs the provision of energy-yielding nutrients to the host animal. Although the predominant species of microbes responsible for ruminal fiber degradation are culturable, the enzymology and genetics underpinning the process are poorly defined. In that context, there were two broad objectives for this proposal. The first objective was to identify the key cellulosomal components in Ruminococcus albus and to characterize their structural features as well as regulation of their expression, in response to polysaccharides and (or) P AA/PPA. The second objective was to evaluate the similarities in the structure and architecture of cellulosomal components between R. albus and other ruminal and non-ruminal cellulolytic bacteria. The cooperation among the investigators resulted in the identification of two glycoside hydrolases rate-limiting to cellulose degradation by Ruminococcus albus (Cel48A and CeI9B) and our demonstration that these enzymes possess a novel modular architecture specific to this bacterium (Devillard et al. 2004). We have now shown that the novel X-domains in Cel48A and Cel9B represent a new type of carbohydrate binding module, and the enzymes are not part of a ceiluiosome-like complex (CBM37, Xu et al. 2004). Both Cel48A and Cel9B are conditionally expressed in response to P AA/PPA, explaining why cellulose degradation in this bacterium is affected by the availability of these compounds, but additional studies have shown for the first time that neither PAA nor PPA influence xylan degradation by R. albus (Reveneau et al. 2003). Additionally, the R. albus genome sequencing project, led by the PI. Morrison, has supported our identification of many dockerin containing proteins. However, the identification of gene(s) encoding a scaffoldin has been more elusive, and recombinant proteins encoding candidate cohesin modules are now being used in Israel to verify the existence of dockerin-cohesin interactions and cellulosome production by R. albus. The Israeli partners have also conducted virtually all of the studies specific to the second Objective of the proposal. Comparative blotting studies have been conducted using specific antibodies prepare against purified recombinant cohesins and X-domains, derived from cellulosomal scaffoldins of R. flavefaciens 17, a Clostridium thermocellum mutant-preabsorbed antibody preparation, or against CbpC (fimbrial protein) of R. albus 8. The data also suggest that additional cellulolytic bacteria including Fibrobacter succinogenes S85, F. intestinalis DR7 and Butyrivibrio fibrisolvens Dl may also employ cellulosomal modules similar to those of R. flavefaciens 17. Collectively, our work during the grant period has shown that R. albus and other ruminal bacteria employ several novel mechanisms for their adhesion to plant surfaces, and produce both cellulosomal and non-cellulosomal forms of glycoside hydrolases underpinning plant fiber degradation. These improvements in our mechanistic understanding of bacterial adhesion and enzyme regulation now offers the potential to: i) optimize ruminal and hindgut conditions by dietary additives to maximize fiber degradation (e.g. by the addition of select enzymes or PAA/PPA); ii) identify plant-borne influences on adhesion and fiber-degradation, which might be overcome (or improved) by conventional breeding or transgenic plant technologies and; iii) engineer or select microbes with improved adhesion capabilities, cellulosome assembly and fiber degradation. The potential benefits associated with this research proposal are likely to be realized in the medium term (5-10 years).
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Stanley-Wall, Nicola, and Joana Carneiro. Life of Bacteria over 200 degrees centigrade: Teachers' Guide. University of Dundee, 2022. http://dx.doi.org/10.20933/100001272.

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The “Life of bacteria over 200 degrees centigrade” video was created by the Public Engagement team at the University of Dundee’s School of Life Sciences, in collaboration with the Nicola-Stanley Wall Lab. This video follows a microbiologist performing an experiment in the laboratory and explains how scientists can study bacteria and biofilms. The video can be used by teachers to show their pupils how some microbial research is done in a professional laboratory environment. This guide helps teachers in this process.
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Myneni, Satish C., Bhoopesh Mishra, and Jeremy Fein. Role of Sulfhydryl Sites on Bacterial Cell Walls in the Biosorption, Mobility and Bioavailability of Mercury and Uranium. Office of Scientific and Technical Information (OSTI), April 2009. http://dx.doi.org/10.2172/1111104.

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Myneni, Satish C. B., Jeremy Fein, and Bhoopesh Mishra. Role of Sulfhydryl Sites on Bacterial Cell Walls in the Biosorption, Mobility and Bioavailability of Mercury and Uranium. Office of Scientific and Technical Information (OSTI), September 2016. http://dx.doi.org/10.2172/1325258.

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Bart, Rebecca. Optimizing tradeoffs implicit during bioenergy crop improvement: Understanding the effect of altered cell wall and sugar content on sorghum-associated pathogenic bacteria. Office of Scientific and Technical Information (OSTI), March 2024. http://dx.doi.org/10.2172/2318644.

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You might also be interested in the extended bibliographies on the topic 'Bacterial wall' for particular source types:
Journal articles Dissertations / Theses Books
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