Ascophyllum and its symbionts. X. Ultrastructure of the interaction between A. nodosum (Phaeophyceae) and Mycophycias ascophylli (Ascomycetes)

Botany ◽  
2008 ◽  
Vol 86 (2) ◽  
pp. 185-193 ◽  
Author(s):  
Haixin Xu ◽  
Ron J. Deckert ◽  
David J. Garbary
Keyword(s):  
Host Cell ◽  
Cortical Cell ◽  
Freeze Substitution ◽  
Host Cells ◽  
Cell Wall Modification ◽  
Transmission Electron ◽  
Host Cell Wall ◽  
Vacuolated Cells ◽  
Cell Preservation

The symbiosis of a brown alga, Ascophyllum nodosum (L.) Le Jolis and its obligate fungal symbiont, Mycophycias ascophylli (Cotton) Kohlmeyer and Volkmann-Kohlmeyer, was studied using transmission electron microscopy. A high quality of cell preservation was achieved after propane-freezing and freeze substitution; this allowed us to observe the interaction of the symbiosis without extensive artifacts. The fungus was found in the middle portion of cortical-cell walls, and at the edge of medullary cells and air-bladder filaments, but never close to host cell protoplasm. Host cell-wall modification was limited to a short distance around the hyphae. A sheath with electron-dense materials around the fungus was found in the older hyphae, but not in the hyphal tips. A range of hyphal ultrastructure was observed from cells with dense cytoplasm, absent to slight vacuolation and with well-defined organelles, to highly vacuolated cells with little cytoplasm and poorly defined organelles, to senescent cells that were often collapsed with no recognizable organelles. No sign of typical cytological resistance responses was observed in host cells, thus confirming the nonantagonistic nature of the two symbionts.

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.

Relations of hyphae to host cells in smut galls caused by species of Tilletia, Tolyposporium, and Ustilago

1987 ◽  
Vol 65 (12) ◽  
pp. 2581-2591 ◽  
Author(s):  
E. S. Luttrell
Keyword(s):  
Host Cell ◽  
Pennisetum Glaucum ◽  
Host Cells ◽  
Smut Fungi ◽  
Differential Growth ◽  
Tilletia Caries ◽  
Transmission Electron ◽  
Infection Threads ◽  
Host Cell Wall ◽  
Host Tissues

Transmission electron microscopy demonstrated that the mycelium in developing galls induced by smut fungi in the Tilletiaceae (Tilletia caries on Triticum aestivum) and Ustilaginaceae (Ustilago nuda on Hordeum vulgare, U. maydis on Zea mays, and Tolyposporium penicillariae on Pennisetum glaucum) may be both intercellular and intracellular. In T. caries the mycelium is mostly intercellular, in U. nuda it is both intercellular and intracellular, and in U. maydis and T. penicillariae it is mostly intracellular. Unconstricted hyphae penetrate the host cell wall, invaginate the host plasmalemma, and become surrounded by a tubular encasement as they cross the host cell. The encasement fuses with the wall on both sides of the host cell, and points of entry and exit have the same appearance. Hyphae traversing host cells resemble infection threads of nodule bacteria. None of these fungi form haustoria. Prior to sporulation masses of hyphae develop in cavities produced by differential growth of host tissues or by disintegration of host cells. Hyphae in such extracellular masses are designated “lacunal hyphae.”

Structure and host–actinomycete interactions in developing root nodules of Comptonia peregrina

1978 ◽  
Vol 56 (5) ◽  
pp. 502-531 ◽  
Author(s):  
William Newcomb ◽  
R. L. Peterson ◽  
Dale Callaham ◽  
John G. Torrey
Keyword(s):  
Host Cell ◽  
Root Nodules ◽  
Host Cells ◽  
Electron Microscopic ◽  
Cortical Cells ◽  
Host Cytoplasm ◽  
Transmission Electron ◽  
Microscopic Studies ◽  
Host Plasma Membrane ◽  
Soil Actinomycete

Correlated fluorescence, bright-field, transmission electron, and scanning electron microscopic studies were made on developing root nodules of Comptonia peregrina (L.) Coult. (Myricaceae) produced by a soil actinomycete which invades the root and establishes a symbiosis leading to fixation of atmospheric dinitrogen. After entering the host via a root hair infection, the hyphae of the endophyte perforate root cortical cells by local degradation of host cell walls and penetration of the host cytoplasm. The intracellular hyphae are always surrounded by host plasma membrane and a thick polysaccharide material termed the capsule. (For convenience, term intracellular refers to the endophyte being inside a Comptonia cell as distinguished from being intercellular, i.e.. between host cells, even though the former is actually extracellular as the endophyte is separated from the host cytoplasm by the host plasmalemma.) Numerous profiles of vesiculate rough endoplasmic reticulum (RER) occur near the growing hyphae. Although the capsule shows a positive Thiery reaction indicating its polysaccharide nature, the fibrillar contents of the RER do not, leaving uncertain whether the capsule results from polymers derived from the RER. Amyloplasts of the cortical cells lose their starch deposits during hyphal proliferation. The hyphae branch extensively in specific layers of the cortex, penetrating much of the host cytoplasm. At this stage, hyphal ends become swollen and form septate club-shaped vesicles within the periphery of the host cells. Lipid-like inclusions and Thiery-positive particles, possibly glycogen, are observed in the hyphae at this time. Associated with hyphal development is an increase in average host cell volume, although nuclear volume appears to remain constant. Concomitant with vesicle maturation, the mitochondrial population increases sharply, suggesting a possible relationship to vesicle function. The intimate interactions between host and endophyte during development of the symbiotic relationship are emphasized throughout.

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.

scholarly journals Listeria monocytogenes: The Impact of Cell Death on Infection and Immunity

Pathogens ◽  
2018 ◽  
Vol 7 (1) ◽  
pp. 8 ◽  
Author(s):  
Courtney McDougal ◽  
John-Demian Sauer
Keyword(s):  
Cell Death ◽  
Listeria Monocytogenes ◽  
Host Cell ◽  
Acute Infection ◽  
Host Cells ◽  
Cell Mediated Immunity ◽  
Cell Death Pathways ◽  
Host Cell Death ◽  
The Impact

Listeria monocytogenes has evolved exquisite mechanisms for invading host cells and spreading from cell-to-cell to ensure maintenance of its intracellular lifecycle. As such, it is not surprising that loss of the intracellular replication niche through induction of host cell death has significant implications on the development of disease and the subsequent immune response. Although L. monocytogenes can activate multiple pathways of host cell death, including necrosis, apoptosis, and pyroptosis, like most intracellular pathogens L. monocytogenes has evolved a series of adaptations that minimize host cell death to promote its virulence. Understanding how L. monocytogenes modulates cell death during infection could lead to novel therapeutic approaches. In addition, as L. monocytogenes is currently being developed as a tumor immunotherapy platform, understanding how cell death pathways influence the priming and quality of cell-mediated immunity is critical. This review will focus on the mechanisms by which L. monocytogenes modulates cell death, as well as the implications of cell death on acute infection and the generation of adaptive immunity.

scholarly journals Evidence for Antibiosis and Induced Host Defense Reactions in the Interaction Between Verticillium lecanii and Penicillium digitatum, the Causal Agent of Green Mold

2000 ◽  
Vol 90 (9) ◽  
pp. 932-943 ◽  
Author(s):  
Nicole Benhamou ◽  
Jacques Brodeur
Keyword(s):  
Plasma Membrane ◽  
Host Cell ◽  
De Novo ◽  
Penicillium Digitatum ◽  
Verticillium Lecanii ◽  
Intercellular Interaction ◽  
Green Mold ◽  
Transmission Electron ◽  
Host Cell Wall ◽  
Host Cell Surface

Chronological events of the intercellular interaction between Verticillium lecanii and the postharvest pathogen Penicillium digitatum were investigated by transmission electron microscopy and gold cytochemistry. Growth inhibition of P. oligandrum as a response to V. lecanii attack correlated with striking host changes including retraction of the plasma membrane and cytoplasm disorganization. Such changes were associated with the deposition on the inner host cell surface of a chitin- and cellulose-enriched material which appeared to be laid down as a structural defense reaction. The accumulation of chitin in the newly formed material correlated with a decrease in the amount of wallbound chitin. However, the deposition of cellulose appeared to correspond to a de novo synthesis, as evidenced by the occurrence of cellulose-containing vesicles which released their content in the space between the invaginated plasma membrane and the host cell wall. Results of the present study provide the first ultrastructural and cytochemical evidence that antagonism, triggered by V. lecanii, is a multifaceted process in which antibiosis, with alteration of the host hyphae prior to contact with the antagonist, appears to be the key process in the antagonism against P. digitatum.

scholarly journals Defining the Mechanical Determinants of Kingella kingae Adherence to Host Cells

2017 ◽  
Vol 199 (23) ◽  
Author(s):  
Brad K. Kern ◽  
Eric A. Porsch ◽  
Joseph W. St. Geme
Keyword(s):  
Host Cell ◽  
High Strength ◽  
Type Iv Pili ◽  
Host Cells ◽  
Initial Contact ◽  
Kingella Kingae ◽  
Content Type ◽  
Type Iv ◽  
Transmission Electron ◽  
Trimeric Autotransporter Adhesin

ABSTRACT Kingella kingae is an important pathogen in young children and initiates infection by colonizing the posterior pharynx. Adherence to pharyngeal epithelial cells is an important first step in the process of colonization. In the present study, we sought to elucidate the interplay of type IV pili (T4P), a trimeric autotransporter adhesin called Knh, and the polysaccharide capsule in K. kingae adherence to host cells. Using adherence assays performed under shear stress, we observed that a strain expressing only Knh was capable of higher levels of adherence than a strain expressing only T4P. Using atomic force microscopy and transmission electron microscopy (TEM), we established that the capsule had a mean depth of 700 nm and that Knh was approximately 110 nm long. Using cationic ferritin capsule staining and thin-section transmission electron microscopy, we found that when bacteria expressing retractile T4P were in close contact with host cells, the capsule was absent at the point of contact between the bacterium and the host cell membrane. In a T4P retraction-deficient mutant, the capsule depth remained intact and adherence levels were markedly reduced. These results support the following model: T4P make initial contact with the host cell and mediate low-strength adherence. T4P retract, pulling the organism closer to the host cell and displacing the capsule, allowing Knh to be exposed and mediate high-strength, tight adherence to the host cell surface. This report provides the first description of the mechanical displacement of capsule enabling intimate bacterial adherence to host cells. IMPORTANCE Adherence to host cells is an important first step in bacterial colonization and pathogenicity. Kingella kingae has three surface factors that are involved in adherence: type IV pili (T4P), a trimeric autotransporter adhesin called Knh, and a polysaccharide capsule. Our results suggest that T4P mediate initial contact and low-strength adherence to host cells. T4P retraction draws the bacterium closer to the host cell and causes the displacement of capsule. This displacement exposes Knh and allows Knh to mediate high-strength adherence to the host cell. This work provides new insight into the interplay of T4P, a nonpilus adhesin, and a capsule and their effects on bacterial adherence to host cells.

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 Dynamic cell wall modifications in brassicas during clubroot disease

2020 ◽  
Author(s):  
Julia Badstöber ◽  
Stefan Ciaghi ◽  
Sigrid Neuhauser
Keyword(s):  
Cell Wall ◽  
Host Cell ◽  
Plasmodiophora Brassicae ◽  
Characteristic Root ◽  
Biotic Interactions ◽  
Microbial Pathogens ◽  
Cell Wall Degrading Enzymes ◽  
Cell Wall Modification ◽  
Clubroot Disease ◽  
Host Cell Wall

AbstractBiotic interactions of plants and microbial pathogens can cause drastic changes in cell wall composition in response to developmental reprogramming caused as consequence of an infection. Clubroot disease, caused by the biotrophic plant pathogen Plasmodiophora brassicae (Phytomyxea, Rhizaria), is the economically most important disease of Brassica crops worldwide. The disease is best known by the characteristic hypertrophied roots (root galls, clubroots). Amongst a series of physiological changes of the host tissue, the formation of the characteristic root galls leads to cell wall modification and reorganization. Cell wall chemistry and the hosts genetic repertoire are discussed to play a role in the resilience of plants against clubroot disease. Plant cells infected with P. brassicae are markedly enlarged, and look very differently from uninfected, healthy cells. Here we systematically review cell wall related processes that lead to the typical clubroot phenotype and provide novel insights how P. brassicae uses these modifications to benefit its own development. An infection with P. brassicae impacts on nearly all cell wall related processes, but all alterations are meaningful for successful growth and development of P. brassicae. Processes related to cell wall stability and rigidity (e.g. cellulose, pectin or lignin synthesis) are down-regulated, while cell wall degrading enzymes or processes that increase the flexibility of the host cell wall (e.g. expansin) are up-regulated. The here presented findings indicate that P. brassicae weakens the structural stability of its host cell while it increases its elasticity, which in consequence allows P. brassicae to grow bigger and ultimately to develop more resting spores. Consequently, the understanding of the modification of the host cell wall is important for the formation of the characteristic root galls but also to better understand clubroot disease.

Ultrastructure of the host-parasite interaction in leaves of Duchesnea indica infected by the rust fungus Frommeëla mexicana var. indicae as revealed by high pressure freezing

2001 ◽  
Vol 79 (1) ◽  
pp. 49-57 ◽  
Author(s):  
C W Mims ◽  
C Rodriguez-Lother ◽  
E A Richardson
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
High Pressure ◽  
Rust Fungus ◽  
Freeze Substitution ◽  
Transfer Cells ◽  
Host Cells ◽  
High Pressure Freezing ◽  
Transmission Electron ◽  
Duchesnea Indica

A combination of scanning and transmission electron microscopy was used to examine the host-pathogen relationship in leaves of Duchesnea indica (Andrz) Focke infected by the rust fungus Frommeëla mexicana var. indicae McCain & Hennen. Samples for transmission electron microscopy were prepared using high pressure freezing followed by freeze substitution. This protocol provided excellent preservation of both host cells and fungal haustoria. Each haustorium of F. mexicana var. indicae possessed a long slender neck with a neck band and an expanded body that contained two nuclei positioned close together. The haustorial body was lobed and sometimes even branched but lacked septa. Details of the extrahaustorial membrane that separated each haustorium from the cytoplasm of its host cell were particularly well preserved. Extensive labyrinth cell wall ingrowths developed around haustorial necks, as well as elsewhere, in infected cells. These ingrowths appeared to be identical to those present in plant transfer cells. Transfer cells are thought to be involved in intensive solute transfer over short distances. This appears to be the first report of the development of transfer cells in response to infection by a plant pathogenic fungus.Key words: haustoria, transfer cells, freeze substitution, electron microscopy.

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