Suppression of host cell wall synthesis at penetration sites in a compatible interaction with a mycoparasite

1985 ◽  
Vol 63 (5) ◽  
pp. 967-973 ◽  
Author(s):  
M. S. Manocha ◽  
C. M. McCullough
Keyword(s):  
Cell Wall ◽  
Host Cell ◽  
Chitin Synthase ◽  
Compatible Interaction ◽  
Cell Wall Synthesis ◽  
Susceptible Host ◽  
Label Incorporation ◽  
Host Cell Wall ◽  
Choanephora Cucurbitarum

Differences in cell wall reactions at the penetration sites on a resistant host, Phascolomyces articulosus Boedijn ex Benny and Benjamin, and on a susceptible host, Choanephora cucurbitarum (Berk. & Rav.) Thaxter, were studied by autoradiography at 18 h after inoculation with a mycoparasite, Piptocephalis virginiana Leadbeater and Mercer. Localized incorporation of a radioactive chitin precursor, N-[3H]acetylglucosamine ([3H]GlcNAc), was observed at the penetration sites on the resistant but not the susceptible host. Autoradiography of mechanically wounded hyphae of the susceptible and resistant hosts showed similar patterns of localized incorporation of [3H]GlcNAc within 5 min after sonication. Label incorporation at the penetration as well as at the wounding sites was inhibited by polyoxin D. Cycloheximide treatment greatly increased the label in subapical regions and reduced that at the hyphal tips in both the hosts, whereas this treatment did not prevent localized incorporation at the wounding or the penetration sites on the resistant host. Suppression of localized incorporation of [3H]GlcNAc at penetration sites in C. cucurbitarum was not due to the lack of mobility of chitin synthase to the penetration site or its activating factor.

Host–parasite relations in mycoparasite. I. Fine structure of host, parasite, and their interface

1971 ◽  
Vol 49 (9) ◽  
pp. 1677-1681 ◽  
Author(s):  
M. S. Manocha ◽  
K. Y. Lee
Keyword(s):  
Cell Wall ◽  
Fine Structure ◽  
Host Cell ◽  
Higher Plants ◽  
Host Cytoplasm ◽  
Host Cell Wall ◽  
Choanephora Cucurbitarum ◽  
A Cell ◽  
Host Parasite

A mycoparasite, Piptocephalis virginiana, shows resemblance to other fungal parasites of higher plants in the fine structure of hyphae and haustoria. The mode of penetration of the host cell, Choanephora cucurbitarum, probably involves mechanical forces. Although the presence of a cell wall degrading enzyme was not detected by conventional techniques, its role in penetration can not be ruled out. A collar around the haustorial neck is formed as an extension of the host cell wall. No papilla was detected although appressorium was seen during penetration. The young haustorium is enclosed in highly invaginating plasmalemma of the host cell and numerous cisternae of endoplasmic reticulum (ER). Appearance of an electron-dense sheath around the mature haustorium seems to coincide with the disappearance of cisternae of ER from the host cytoplasm in the vicinity of the haustorium. The role of host cytoplasm, particularly of ER, in the development of the sheath is discussed. Extensive accumulation of spherosome-like bodies, containing lipids, is found in haustorium, parasite, and host hypha.

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.

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.

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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