Abstract P-6: Automated Pipeline for Parametrization of the Coarse-Grained Models for Biomolecular Simulations

Background: Antibiotic-resistant strains of Staphylococcus aureus cause human infections that are difficult to treat and can lead to death. Bacteriophage (phage) phi812K1/420 from the family Myoviridae infects 95% of clinical isolates of S. aureus and therefore is a promising candidate for a phage therapy agent. As the native phage particle approaches its host cell, phage receptor-binding proteins make a contact with the host cell wall. This interaction triggers a cascade of structural changes in the baseplate resulting in phage tail contraction and genome ejection. Mechanistic description of the baseplate re-organization, however, remains unknown. Methods: Using cryo-electron microscopy (cryo-EM), we studied the baseplate of the phage phi812K1/420. Also, selected proteins involved in the host cell wall binding and penetration were produced in recombinant form and their structures were solved using X-ray crystallography and cryo-EM single-particle reconstruction. Results: We reconstructed the phage baseplate in native and contracted states. The reconstruction of the native baseplate reaches a resolution of 4 Å, which enables us to discern individual protein structures. Solved protein structures will be fitted into the reconstruction of the contracted baseplate. Conclusion: Our results provide the first structural characterization of contractile phage infecting a Gram-positive bacterium. Comparison of the two distinct baseplate states will allow us to describe the molecular mechanism of the initial stage of phage infection in detail.

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Investigation of the Relationship between Lactococcal Host Cell Wall Polysaccharide Genotype and 936 Phage Receptor Binding Protein Phylogeny

Applied and Environmental Microbiology ◽

10.1128/aem.00653-13 ◽

2013 ◽

Vol 79 (14) ◽

pp. 4385-4392 ◽

Cited By ~ 70

Author(s):

J. Mahony ◽

W. Kot ◽

J. Murphy ◽

S. Ainsworth ◽

H. Neve ◽

...

Keyword(s):

Cell Wall ◽

Host Cell ◽

Receptor Binding ◽

Binding Protein ◽

Cell Wall Polysaccharide ◽

Protein Phylogeny ◽

Host Cell Wall ◽

Phage Receptor ◽

The Relationship ◽

Receptor Binding Protein

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Studies on the infection process of Fusarium culmorum in wheat spikes: Degradation of host cell wall components and localization of trichothecene toxins in infected tissue

Mycotoxins in Plant Disease ◽

10.1007/978-94-010-0001-7_7 ◽

2002 ◽

pp. 653-660 ◽

Cited By ~ 1

Author(s):

Z. Kang ◽

H. Buchenauer

Keyword(s):

Cell Wall ◽

Host Cell ◽

Fusarium Culmorum ◽

Infection Process ◽

Infected Tissue ◽

Cell Wall Components ◽

Host Cell Wall ◽

Wall Components

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Comparative Transcriptomic Analysis of Race 1 and Race 4 of Fusarium oxysporum f. sp. cubense Induced with Different Carbon Sources

G3 Genes|Genome|Genetics ◽

10.1534/g3.117.042226 ◽

2017 ◽

Vol 7 (7) ◽

pp. 2125-2138 ◽

Cited By ~ 4

Author(s):

Shiwen Qin ◽

Chunyan Ji ◽

Yunfeng Li ◽

Zhenzhong Wang

Keyword(s):

Gene Expression ◽

Cell Wall ◽

Fusarium Oxysporum ◽

Host Cell ◽

Expression Profiles ◽

Cell Wall Polysaccharide ◽

Host Cell Wall ◽

Race 1 ◽

Race 4 ◽

Banana Cultivar

Abstract The fungal pathogen Fusarium oxysporum f. sp. cubense causes Fusarium wilt, one of the most destructive diseases in banana and plantain cultivars. Pathogenic race 1 attacks the “Gros Michel” banana cultivar, and race 4 is pathogenic to the Cavendish banana cultivar and those cultivars that are susceptible to Foc1. To understand the divergence in gene expression modules between the two races during degradation of the host cell wall, we performed RNA sequencing to compare the genome-wide transcriptional profiles of the two races grown in media containing banana cell wall, pectin, or glucose as the sole carbon source. Overall, the gene expression profiles of Foc1 and Foc4 in response to host cell wall or pectin appeared remarkably different. When grown with host cell wall, a much larger number of genes showed altered levels of expression in Foc4 in comparison with Foc1, including genes encoding carbohydrate-active enzymes (CAZymes) and other virulence-related genes. Additionally, the levels of gene expression were higher in Foc4 than in Foc1 when grown with host cell wall or pectin. Furthermore, a great majority of genes were differentially expressed in a variety-specific manner when induced by host cell wall or pectin. More specific CAZymes and other pathogenesis-related genes were expressed in Foc4 than in Foc1 when grown with host cell wall. The first transcriptome profiles obtained for Foc during degradation of the host cell wall may provide new insights into the mechanism of banana cell wall polysaccharide decomposition and the genetic basis of Foc host specificity.

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Extracellular Polysaccharides from Xanthomonas axonopodis pv. manihotis Interact with Cassava Cell Walls During Pathogenesis

Molecular Plant-Microbe Interactions ◽

10.1094/mpmi.1997.10.7.803 ◽

1997 ◽

Vol 10 (7) ◽

pp. 803-811 ◽

Cited By ~ 23

Author(s):

B. Boher ◽

M. Nicole ◽

M. Potin ◽

J. P. Geiger

Keyword(s):

Cell Wall ◽

Monoclonal Antibodies ◽

Host Cell ◽

Cell Walls ◽

Plant Cell Wall ◽

Infection Process ◽

Extracellular Polysaccharides ◽

Xanthomonas Axonopodis ◽

Cassava Leaves ◽

Host Cell Wall

The location of lipopolysaccharides produced by Xanthomonas axonopodis pv. manihotis during pathogenesis on cassava (Manihot esculenta) was determined by fluorescence and electron microscopy immunolabeling with monoclonal antibodies. During the early stages of infection, pathogen lipopolysaccharides were detected on the outer surface of the bacterial envelope and in areas of the plant middle lamellae in the vicinity of the pathogen. Later in the infection process, lipopolysaccharide-specific antibodies bound to areas where the plant cell wall was heavily degraded. Lipopolysaccharides were not detected in the fibrillar matrix filling intercellular spaces of infected cassava leaves. Monoclonal antibodies specific for the exopolysaccharide xanthan side chain labeled the bacteria, the fibrillar matrix, and portions of the host cell wall. The association of Xanthomonas lipopolysaccharides with host cell walls during plant infection is consistent with a role of these bacterial extracellular polysaccharides in the infection process.

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Ultrastructure of compatible and incompatible reactions of sunflower to Plasmopara halstedii

Canadian Journal of Botany ◽

10.1139/b79-043 ◽

1979 ◽

Vol 57 (4) ◽

pp. 315-323 ◽

Cited By ~ 15

Author(s):

Glenn Wehtje ◽

Larry J. Littlefield ◽

David E. Zimmer

Keyword(s):

Cell Wall ◽

Plasma Membrane ◽

Host Cell ◽

Epidermal Cell ◽

Cortical Cell ◽

Hypersensitive Reaction ◽

Host Cells ◽

Plasmopara Halstedii ◽

Host Cell Wall ◽

Host Plasma Membrane

Penetration of sunflower, Heliantluis animus, root epidermal cells by zoospores of Plasmopara halstedii is preceded by formation of a papilla on the inner surface of the host cell wall that invaginates the host plasma membrane. Localized degradation and penetration of the host cell wall by the pathogen follow. The invading fungus forms an allantoid primary infection vesicle in the penetrated epidermal cell. The host plasma membrane invaginates around the infection vesicle but its continuity is difficult to follow. Upon exit from the epidermal cell the fungus may grow intercellularly, producing terminal haustorial branches which extend into adjacent host cells. The fungus may grow through one or two cortical cell is after growing from the epidermal cell before it becomes intercellular. Host plasma membrane is not penetrated by haustoria. Intercellular hyphae grow toward the apex of the plant and ramify the seedling tissue. Resistance in an immune cultivar is hypersensitive and is triggered upon contact of the host cell with the encysting zoospore before the host cell wall is penetrated. Degeneration of zoospore cytoplasm accompanies the hypersensitive reaction of the host. Zoospores were often parasitized by bacteria and did not germinate unless penicillin and streptomycin were added to the inoculum suspension.

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Host cell wall synthesis and its role in resistance to a mycoparasite

Physiological Plant Pathology ◽

10.1016/0048-4059(82)90081-9 ◽

1982 ◽

Vol 20 (2) ◽

pp. 157-164 ◽

Cited By ~ 7

Author(s):

M.S. Manocha ◽

Lori L. Graham

Keyword(s):

Cell Wall ◽

Host Cell ◽

Cell Wall Synthesis ◽

Host Cell Wall

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Histopathology of Fusarium wilt of staghorn sumac (Rhus typhina) caused by Fusarium oxysporum f. sp. callistephi race 3. III. Host cell and tissue reactions

Phytoprotection ◽

10.7202/013967ar ◽

2006 ◽

Vol 87 (1) ◽

pp. 17-27 ◽

Cited By ~ 3

Author(s):

Guillemond B. Ouellette ◽

Mohamed Cherif ◽

Marie Simard

Keyword(s):

Cell Wall ◽

Fusarium Oxysporum ◽

Host Cell ◽

Cross Wall ◽

Tissue Proliferation ◽

Host Cytoplasm ◽

Transmission Electron ◽

Host Cell Wall ◽

Tissue Reactions ◽

Rhus Typhina

Abstract Various cell reactions occurred in staghorn sumac plants inoculated with Fusarium oxysporum f. sp. callistephi. Light and transmission electron microscopy observations and results of cytochemical tests showed: 1) increased laticifers and latex production in the phloem; 2) tylosis formation; 3) host cell wall modifications, including appositions or other cell wall thickenings; and 4) unusual cross wall formation in some cells, and cell hypertrophy and hyperplasia. Tylosis walls labelled for pectin and cellulose and many displayed inner suberin-like layers. These layers were also noted in cells of the medullary sheath and in many cells with dense content and thickened walls in the barrier zones that had formed. These zones also contained fibres with newly-formed gelatinous-like layers. In the vicinity of these cells, host cell walls were frequently altered, associated with opaque matter. Many small particles present in chains also occurred in some of these cells, which contained only remnants of host cytoplasm. Light microscopy observations showed that pronounced tissue proliferation and aberrant cells occurred in the outer xylem in the infected plants. Unusual neoplasmic tissue also formed from cells surrounding the pith and medullary sheath, and it spanned directly across the pre-existing xylem tissue and burst as large mounds on the stems.

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