Axenic culture of flax rust isolated from cotyledons by cell-wall digestion

1972 ◽  
Vol 50 (12) ◽  
pp. 2601-2603 ◽  
Author(s):  
W. David Lane ◽  
Michael Shaw
Keyword(s):  
Cell Wall ◽  
Host Cell ◽  
Cell Walls ◽  
Hydrolytic Enzymes ◽  
Axenic Culture ◽  
Rust Fungi ◽  
Host Cells ◽  
Melampsora Lini ◽  
Large Numbers ◽  
Axenic Cultures

A technique is described for the isolation of colonies of flax rust (Melampsora lini (Ehrenb.) Lév., Race No. 3) from infected cotyledons. The technique depends on the digestion of the host cell walls with hydrolytic enzymes and washing of the liberated colonies. It is thus possible to collect large numbers of flax-rust colonies with only a few host cells adhering to them. Axenic cultures were established from colonies isolated in this way. This technique may be useful in establishing axenic cultures of other rust fungi.

scholarly journals Histology of Infection of Hydrilla verticillata by Macrophomina phaseolina

Weed Science ◽  
1992 ◽  
Vol 40 (2) ◽  
pp. 288-295 ◽  
Author(s):  
Gary F. Joye ◽  
Rex N. Paul
Keyword(s):  
Cell Wall ◽  
Host Cell ◽  
Epidermal Cell ◽  
Cell Walls ◽  
Hydrilla Verticillata ◽  
Macrophomina Phaseolina ◽  
Host Cells ◽  
Outer Cell ◽  
Cell Wall Disruption ◽  
Outer Cell Wall

Infection of Hydrilla verticillata by Macrophomina phaseolina was investigated using scanning and transmission electron microscopy. Sprigs of plants in petri plates were inoculated with suspensions of fungal hyphae. Samples of inoculated and noninoculated plants were taken over time. Fungal cells attached to lower epidermal cell walls but not the upper epidermal cell walls of leaves. In less than 40 h, penetration through the cell wall was completed and colonization of host cells was observed. Penetration of upper epidermis was limited to the cell wall adjacent to a lower epidermal cell. No penetration was observed through the outer cell wall of upper epidermis. Inhibition of penetration through the outer cell wall of the upper epidermis may be attributable to an osmiophilic layer below the cell wall. Disruption of the host cell walls and subsequent host cell death was preceded by massive colonization of the host by this pathogen.

Changes of plasmolysis form in epidermal cells of Hordeum vulgare infected by Erysiphe graminis: evidence for increased membrane–wall adhesion

1984 ◽  
Vol 62 (8) ◽  
pp. 1714-1723 ◽  
Author(s):  
O. Y. Lee-Stadelmann ◽  
W. R. Bushnell ◽  
E. J. Stadelmann
Keyword(s):  
Cell Wall ◽  
Hordeum Vulgare ◽  
Host Cell ◽  
Cell Walls ◽  
Membrane Structure ◽  
Epidermal Cells ◽  
Erysiphe Graminis ◽  
Infected Tissue ◽  
Host Cells

When coleoptile epidermal tissues of Hordeum vulgare were plasmolyzed with α-methylglucose or mannitol, 24–72 h after inoculation with Erysiphe graminis f. sp. hordei, host protoplasts tended to pull away from one or more sites on longitudinal host cell walls producing a concave pocket at each site. This contrasted with the usual convex form of plasmolysis in uninfected tissue in which protoplasts pulled from the short transversal end walls of host cells forming protoplasts with convex ends. The tendency for concave plasmolysis encompassed entire inoculated areas at 5 colonies/mm2 and above. The concave response occurred in coleoptiles inoculated 7–12 days after planting, but not in ones inoculated at 5 days. It occurred in four of five barley lines tested at 48 h postinoculation. Treatment before plasmolysis with 10 mM Ca2+ promoted the disease-induced concavities; treatment with 15 mM K+ partially inhibited them. The concave form in plasmolyzed infected tissue was changed to the convex form by addition of 250 μM octylguanidine to the plasmolyticum or by replacement of α-methylglucose with isosmolar urea or methyl urea solutions. The results suggest that Erysiphe graminis infection increased adhesion of the host plasmalemma to the cell wall, probably as a consequence of change in membrane structure and bridging by Ca2+ ions.

Studies on the haustorium of Castilleja (Scrophulariaceae). II. The endophyte

1973 ◽  
Vol 51 (5) ◽  
pp. 923-931 ◽  
Author(s):  
David R. Dobbins ◽  
Job Kuijt
Keyword(s):  
Cell Wall ◽  
Host Cell ◽  
Light Microscope ◽  
Cell Walls ◽  
Host Cells ◽  
Electron Microscopic ◽  
Cortical Cells ◽  
Host Cell Wall ◽  
Dark Staining ◽  
Host Tissues

The portion of the Castilleja haustorium within the host, the endophyte, was examined at the light-and electron-microscopic levels. The endophyte consists of a stalk of lipid-containing cells and digitate cells at its tip. Vessels run the length of the endophyte. There is a harmonious meshing between host cortical cells and those of the endophyte flank, suggesting that penetration is accomplished, in part, by cell dissolution. Crushing of cells also occurs during endophyte invasion as host phloem tissues are severely buckled and cell walls are greatly folded. Some features of digitate cells include dense cytoplasm, an abundance of endoplasmic reticulum, lateral walls that are thickened as well as those on the side adjacent to the host, and an ability to conform to the contours of host tissues. Often digitate cells are divided by very thin walls that are hardly visible under the light microscope. It is suggested that the thick cell walls may function as "free space" in the absorption of materials from the host. Within the endophyte, vessels differentiate and may contain either a finely granular, dark-staining material or a more coarsely granular, light-staining material. The particles of the latter have irregular shapes. Although granular materials are thus carried by some vessels, cells resembling the structurally intermediate "phloeotracheids" were not seen. Connections through the cell wall were not observed between parasite and host; however, within the endophyte plasmodesmata were highly branched and often contained median nodules. Transfer-like cells which have irregularly thickened walls occurred in the endophyte. Host tissues next to digitate cells appeared to be in a degraded state. Invaginations of the plasmalemma were common and small flattened vesicles were formed in some host cells from the disrupted tonoplast. In several instances, the cytoplasm had receded from the host cell wall and a "beaded" material was present in both vacuoles and large vesicles. The host cell wall at times had a very loose fibrillar appearance. Some host tracheids were occluded with a dense and dark-staining material. The xylem strands of the parasite are connected to the host xylem either by cell wall dissolution or by actual penetration of a digitate cell into a host xylary cell. The penetrating cell subsequently differentiates into a vessel member. A summary and general discussion are given to relate the two portions of the haustorium, the upper haustorium and the endophyte. The mass of new information gained in this study leads us to encourage the application of plastic embedding and sectioning techniques to further light-microscope studies on haustoria.

Colony initiation in flax rust in axenic culture: involvement of a volatile factor

1979 ◽  
Vol 57 (23) ◽  
pp. 2657-2662 ◽  
Author(s):  
Rosalinda Boasson ◽  
Michael Shaw
Keyword(s):  
Carbon Dioxide ◽  
Axenic Culture ◽  
Conclusive Evidence ◽  
Culture Flask ◽  
Melampsora Lini ◽  
Air Space ◽  
Lag Period ◽  
Axenic Cultures ◽  
Incubation Temperatures

In axenic cultures of flax rust (Melampsora lini) colonies are initiated after a lag period of 12–20 days, depending partly on incubation temperatures. Colony initiation is completely inhibited by removal of a volatile factor which is absorbed by KOH in the air space of the culture flask. The fungus remains sensitive to this inhibition for 8–10 days, i.e., until shortly before visible colonies would normally have developed. While in the presence of KOH, the fungus is not killed; cultures grow normally after removal of the KOH.Although conclusive evidence must await further work, the available data strongly suggest that carbon dioxide is responsible for this effect.

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

1997 ◽  
Vol 10 (7) ◽  
pp. 803-811 ◽  
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.

Ultrastructure of compatible and incompatible reactions of sunflower to Plasmopara halstedii

1979 ◽  
Vol 57 (4) ◽  
pp. 315-323 ◽  
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.

scholarly journals Identification of a Chlorovirus PBCV-1 Protein Involved in Degrading the Host Cell Wall during Virus Infection

Viruses ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 782
Author(s):  
Irina V. Agarkova ◽  
Leslie C. Lane ◽  
David D. Dunigan ◽  
Cristian F. Quispe ◽  
Garry A. Duncan ◽  
...  
Keyword(s):  
Cell Wall ◽  
Host Cell ◽  
Cell Walls ◽  
Virus Entry ◽  
Cell Type ◽  
Chlorella Variabilis ◽  
Rigid Cell Wall ◽  
Host Cell Wall ◽  
Cell Type Specific ◽  
Eukaryotic Organisms

Chloroviruses are unusual among viruses infecting eukaryotic organisms in that they must, like bacteriophages, penetrate a rigid cell wall to initiate infection. Chlorovirus PBCV-1 infects its host, Chlorella variabilis NC64A by specifically binding to and degrading the cell wall of the host at the point of contact by a virus-packaged enzyme(s). However, PBCV-1 does not use any of the five previously characterized virus-encoded polysaccharide degrading enzymes to digest the Chlorella host cell wall during virus entry because none of the enzymes are packaged in the virion. A search for another PBCV-1-encoded and virion-associated protein identified protein A561L. The fourth domain of A561L is a 242 amino acid C-terminal domain, named A561LD4, with cell wall degrading activity. An A561LD4 homolog was present in all 52 genomically sequenced chloroviruses, infecting four different algal hosts. A561LD4 degraded the cell walls of all four chlorovirus hosts, as well as several non-host Chlorella spp. Thus, A561LD4 was not cell-type specific. Finally, we discovered that exposure of highly purified PBCV-1 virions to A561LD4 increased the specific infectivity of PBCV-1 from about 25–30% of the particles forming plaques to almost 50%. We attribute this increase to removal of residual host receptor that attached to newly replicated viruses in the cell lysates.

scholarly journals Biosynthesis and Virulent Behavior of Lipids Produced by Mycobacterium tuberculosis: LAM and Cord Factor: An Overview

2011 ◽  
Vol 2011 ◽  
pp. 1-7 ◽  
Author(s):  
Rajni ◽  
Nisha Rao ◽  
Laxman S. Meena
Keyword(s):  
Cell Wall ◽  
Mycobacterium Tuberculosis ◽  
Host Cell ◽  
Phosphatidyl Inositol ◽  
Polymorphonuclear Neutrophils ◽  
Host Cells ◽  
Wall Structure ◽  
Trehalose Dimycolate ◽  
Cell Immunity ◽  
Cord Factor

Mycobacterium tuberculosis is the causative agent of tuberculosis disease, which has developed a myriad of exceptional features contributing to its survival within the hostile environment of host cell. Unique cell wall structure with high lipid content plays an imperative role in the pathogenicity of mycobacteria. Cell wall components of MTB such as lipoarabinomannan and Trehalose dimycolate (cord factor) are virulent in nature apart from its virulence genes. Virulent effect of these factors on host cells reduces host cell immunity. LAM has been known to inhibit phagosome maturation by inhibiting the Ca2+/calmodulin phosphatidyl inositol-3-kinase hvps34 pathways. Moreover, TDM (Trehalose dimycolate) also inhibits fusion between phospholipid vesicles and migration of polymorphonuclear neutrophils. The objective of this paper is to understand the virulence of LAM and cord factor on host cell which might be helpful to design an effective drug against tuberculosis.

Schizophyllum commune Fr. as a destructive mycoparasite

1978 ◽  
Vol 24 (7) ◽  
pp. 780-784 ◽  
Author(s):  
S. S. Tzean ◽  
R. H. Estey
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Host Cell ◽  
Cell Walls ◽  
Schizophyllum Commune ◽  
Host Cells ◽  
Transmission Electron ◽  
Reaction Region

Schizophyllum commune Fr. was shown, by light, scanning, and transmission electron microscopy, to be a destructive mycoparasite on several phytopathogenic and nematode-trapping fungi. The hyphae of S. commune coiled around host hyphae and fruiting structures and penetrated them by means of either unspecialized hyphae or by penetration pegs that developed from terminal appressoria. The host cell walls were usually chemically degraded after which the parasite grew through an electron-dense, papillate, reaction region and its underlying membrane(s) to produce trophic hyphae inside the host cells.

scholarly journals Chitinases Are Essential for Sexual Development but Not Vegetative Growth in Cryptococcus neoformans

2009 ◽  
Vol 8 (11) ◽  
pp. 1692-1705 ◽  
Author(s):  
Lorina G. Baker ◽  
Charles A. Specht ◽  
Jennifer K. Lodge
Keyword(s):  
Cell Wall ◽  
Sexual Reproduction ◽  
Cryptococcus Neoformans ◽  
Vegetative Growth ◽  
Cell Walls ◽  
Cell Structure ◽  
Complex Structure ◽  
Hydrolytic Enzymes ◽  
Fungal Cell ◽  
Fungal Cell Walls

ABSTRACT Cryptococcus neoformans is an opportunistic pathogen that mainly infects immunocompromised individuals. The fungal cell wall of C. neoformans is an excellent target for antifungal therapies since it is an essential organelle that provides cell structure and integrity. Importantly, it is needed for localization or attachment of known virulence factors, including melanin, phospholipase, and the polysaccharide capsule. The polysaccharide fraction of the cryptococcal cell wall is a complex structure composed of chitin, chitosan, and glucans. Chitin is an indispensable component of many fungal cell walls that contributes significantly to cell wall strength and integrity. Fungal cell walls are very dynamic, constantly changing during cell division and morphogenesis. Hydrolytic enzymes, such as chitinases, have been implicated in the maintenance of cell wall plasticity and separation of the mother and daughter cells at the bud neck during vegetative growth in yeast. In C. neoformans we identified four predicted endochitinases, CHI2, CHI21, CHI22, and CHI4, and a predicted exochitinase, hexosaminidase, HEX1. Enzymatic analysis indicated that Chi2, Chi22, and Hex1 actively degraded chitinoligomeric substrates. Chi2 and Hex1 activity was associated mostly with the cellular fraction, and Chi22 activity was more prominent in the supernatant. The enzymatic activity of Hex1 increased when grown in media containing only N-acetylglucosamine as a carbon source, suggesting that its activity may be inducible by chitin degradation products. Using a quadruple endochitinase deletion strain, we determined that the endochitinases do not affect the growth or morphology of C. neoformans during asexual reproduction. However, mating assays indicated that Chi2, Chi21, and Chi4 are each involved in sexual reproduction. In summary, the endochitinases were found to be dispensable for routine vegetative growth but not sexual reproduction.

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