scholarly journals Cellular interaction of the smut fungus Ustacystis waldsteiniae

1995 ◽  
Vol 73 (6) ◽  
pp. 867-883 ◽  
Author(s):  
Robert Bauer ◽  
Franz Oberwinkler ◽  
Kurt Mendgen
Keyword(s):  
High Pressure ◽  
Cell Wall ◽  
Plasma Membrane ◽  
Host Cell ◽  
Smut Fungus ◽  
Cellular Interaction ◽  
Smut Fungi ◽  
The Matrix ◽  
Host Cell Wall ◽  
Host Plasma Membrane

The cellular interaction between the smut fungus Ustacystis waldsteiniae and its host Waldsteinia geoides was analyzed by serial-section electron microscopy using chemically fixed and high-pressure frozen – freeze-substituted samples. After penetration, each haustorium extends a short distance into the host cell where it often forms up to three short lobes. The haustorium is wholly ensheathed by a prominent matrix. The matrix is a complex structure, differing significantly from that known of other fungal plant parasites: it is filled with amorphous, electron-opaque material in which membrane-bounded, coralloid vesicles are embedded. During the contact phase of the hypha with the host cell wall, vesicles with electron-opaque contents accumulate in the contact area of the hypha where they appear to fuse with the fungal plasma membrane and extrude their contents. Subsequently, the host cell wall increases in electron opacity and matrix material becomes deposited between host plasma membrane and host cell wall exactly at the ends of the altered areas in the host cell wall. The coralloid vesicles within the matrix, however, are of host origin: exocytosis of Golgi products into the matrix results in the formation of coralloid vesicular buds in the host plasma membrane. Subsequently, the buds seem to detach from the host plasma membrane to flow as coralloid vesicles into the matrix. Matrix development continues during penetration and after penetration at the haustorial tips. After host wall penetration, the fungal cell wall comes in contact with the matrix. The fungal component of the matrix may play a key role in the inducement of these transfer cell-like compartments in host cells responding to infection. Key words: freeze substitution, haustoria, high-pressure freezing, host–parasite interaction, smut fungi, Ustacystis waldsteiniae.

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 Lactococcal Bacteriophages Require a Host Cell Wall Carbohydrate and a Plasma Membrane Protein for Adsorption and Ejection of DNA

1994 ◽  
Vol 60 (9) ◽  
pp. 3204-3211 ◽  
Author(s):  
Marshall R. Monteville ◽  
Bahram Ardestani ◽  
Bruce L. Geller
Keyword(s):  
Cell Wall ◽  
Plasma Membrane ◽  
Membrane Protein ◽  
Host Cell ◽  
Plasma Membrane Protein ◽  
Host Cell Wall

An electron microscope study of the intracellular hyphae of some smut fungi (Ustilaginales)

1970 ◽  
Vol 18 (3) ◽  
pp. 285 ◽  
Author(s):  
RA Fullerton
Keyword(s):  
Cell Wall ◽  
Electron Microscope ◽  
Host Cell ◽  
Microscope Study ◽  
Electron Microscope Study ◽  
Smut Fungi ◽  
Sheath Formation ◽  
Host Cell Wall ◽  
Similar Appearance ◽  
Host Tissues

A number of species of systemic smut fungi have been examined. Hyphae occupy inter- and intracellular positions in the host tissues. Intracellular hyphae resemble haustoria in many respects. Host plasmalemmae are invaginated by invading hyphae, and encapsulations are formed. Material of similar appearance to the host cell wall is deposited within encapsulations and many hyphae are eventually completely ensheathed. A possible mechanism for sheath formation is suggested.

Ultrastructure of the host–pathogen interface in Arabidopsis thaliana leaves infected by the downy mildew Hyaloperonospora parasitica

2004 ◽  
Vol 82 (7) ◽  
pp. 1001-1008 ◽  
Author(s):  
C W Mims ◽  
E A Richardson ◽  
B F Holt III ◽  
J L Dangl
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Arabidopsis Thaliana ◽  
High Pressure ◽  
Cell Wall ◽  
Host Cell ◽  
Hyaloperonospora Parasitica ◽  
Transmission Electron ◽  
Host Pathogen ◽  
Host Cell Wall

Transmission electron microscopy was used to examine the host–pathogen interface in Arabidopsis thaliana (L.) Heynh. leaves infected by the biotrophic downy mildew pathogen Hyaloperonospora parasitica (Pers.:Fr.) Constant. Both conventionally fixed as well as high-pressure frozen samples were examined. Excellent preservation of the host–pathogen interface was obtained in many of our high-pressure frozen samples and provided information not available in conventionally fixed samples. Mature haustoria of H. parasitica were distinctly pyriform in shape. A small collar of host cell wall material surrounded the neck of each haustorium near the host cell wall penetration site. The presence of callose in collars was demonstrated using immunogold labeling with a monoclonal antibody specific for (1→3)-β-glucans. The body of each haustorium was ensheathed by an invaginated portion of the invaded host-cell plasma membrane known as the extrahaustorial membrane. Lying between this membrane and the haustorial wall was a layer of electron-dense material known as the extrahaustorial matrix (EHM). The EHM typically was thicker at the distal end of a haustorium than at the proximal end. The surface of the EHM covered by the extrahaustorial membrane was highly irregular in outline. Considerable vesicular activity was observed in association with the extrahaustorial membrane.Key words: transmission electron microscopy, high-pressure freezing, haustoria, Peronospora parasitica.

Ultrastructure of Haustoria of Plant Pathogenic Fungi

1998 ◽  
Vol 4 (S2) ◽  
pp. 1140-1141
Author(s):  
C. W. Mims ◽  
E. A. Richardson
Keyword(s):  
Plasma Membrane ◽  
Host Cell ◽  
Pathogenic Fungi ◽  
Life Cycles ◽  
Plant Pathogenic Fungi ◽  
Obligate Parasites ◽  
Cell Plasma ◽  
Different Types ◽  
Host Cell Wall ◽  
Host Plasma Membrane

Most plant pathogenic fungi that are obligate parasites produce haustoria which are thought to be involved in nutrient absorption. A haustorium is a specialized hyphal branch that penetrates the host cell wall and invaginates the host cell plasma membrane. The host plasma membrane ensheathing the haustorium is termed the extrahaustorial membrane. This presentation provides examples of different types of haustoria produced by plant pathogenic fungi. Species considered here are 1) Cronartium quercuum f. sp.fusiforme, the cause of fusiform gall rust of pine, 2) Puccinia arachidis, the cause of peanut rust1, 3) Uncinuliella australiana, the cause of powdery mildew of crape myrtle, 4) Exobasidium camelliae, a pathogen of Camellia sasanqua2, and 5) Cercosporidium personatum, the cause of late leaf spot of peanut.Rust fungi typically require two different host species to complete their life cycles. The dikaryotic phase of the rust life cycle consists of intercellular hyphae that give rise to specialized haustoria known as D-haustoria which are remarkably similar from one species to the next.

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

2017 ◽  
Vol 7 (7) ◽  
pp. 2125-2138 ◽  
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.

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.

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

1982 ◽  
Vol 20 (2) ◽  
pp. 157-164 ◽  
Author(s):  
M.S. Manocha ◽  
Lori L. Graham
Keyword(s):  
Cell Wall ◽  
Host Cell ◽  
Cell Wall Synthesis ◽  
Host Cell Wall

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

2006 ◽  
Vol 87 (1) ◽  
pp. 17-27 ◽  
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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