An ultrastructural study of the marine diatom Licmophora hyalina and its parasite Ectrogella perforons. I. Infection of host cells

1980 ◽  
Vol 58 (11) ◽  
pp. 1280-1290 ◽  
Author(s):  
Chandralata Raghu Kumar
Keyword(s):  
Plasma Membrane ◽  
Germ Tube ◽  
Host Cells ◽  
Marine Diatom ◽  
Electron Microscopic ◽  
Fungal Parasite ◽  
Successful Infection ◽  
Host Cell Wall ◽  
Host Plasma Membrane ◽  
Host Parasite

An electron microscopic study has been made on the infection and penetration of the marine diatom Licmophora hyalina Agardh by Ectrogella perforons Petersen, an obligate fungal parasite of diatoms. The zoospores encyst on the host cell wall. The nucleus of the cyst may be situated proximal or distal to the host wall. A germ tube is produced from the side where the nucleus is situated. The germ tube may be branched or unbranched. The penetrating germ tube swells distally, develops an appressorium at the site of penetration of the host wall, and pierces the host wall in the form of an infection peg. The infection peg is smaller in diameter than the germ tube and the appressorium. Successful infection takes place always at the areolae of the diatom wall. The infection peg may directly inject its contents by piercing the subfrustular layer of the diatom wall or may grow for some distance beneath the subfrustular layer. At the site of entry the host plasma membrane invaginates and surrounds the fungal protoplast. Initially, the host–parasite interface consists of a two-layered envelope of which the outer one is the host plasma membrane and the inner one the fungal plasma membrane.

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.

Host – parasite relationships between the fungus Leptosphaerulina crassiasca and peanut

1992 ◽  
Vol 70 (9) ◽  
pp. 1724-1733 ◽  
Author(s):  
Mei-Lee Wu ◽  
Richard T. Hanlin
Keyword(s):  
Cell Wall ◽  
Host Cell ◽  
Germ Tube ◽  
Light And Electron Microscopy ◽  
Host Cells ◽  
Detached Leaves ◽  
Host Cell Wall ◽  
Host Parasite ◽  
Germ Tubes ◽  
Infection Hypha

The mode of penetration and infection of the peanut leaf by Leptosphaerulina crassiasca were studied by means of light and electron microscopy. The attachment of the multicellular ascospores to the leaf surface was by a mucilagenous sheath that covered the ascospores at maturity. This sheath expanded rapidly in moisture and it extended along the germ tube as it elongated. Two types of germ tubes appeared to be formed, a short one and a relatively long one. Short germ tubes were not delimited by septa, and they penetrated the cuticle and host epidermal cell wall directly without appressorium formation. Penetration occurred 2–6 h after inoculation. The wall was breached by a relatively broad infection hypha that expanded in width inside the host cell wall. The lack of mechanical rupture at the infection site indicated that penetration may involve enzymatic activity. Intracellular hyphae were present in the epidermal cells, but only intercellular hyphae occurred in the palisade and spongy mesophyll tissues. The intercellular hyphae were frequently appressed to the outer surface of the host cell wall. Infected areas rarely exceeded 1 mm in diameter, and they were only sparsely colonized by hyphae of the pathogen. Host cells in the vicinity of hyphae underwent senescence and death. One to 2 months after inoculation, pseudothecia formed in the dead tissues of detached leaves. In some instances the presence of penetration hyphae by short germ tubes induced the formation of a papilla inside the host cell wall, which either restricted growth of the infection hypha or resulted in the death of the germ tube and the cell from which it arose. Long germ tubes were delimited by simple septa and they terminated in an appressorium; however, details of their behavior were not studied. Key words: Arachis hypogaea, Ascomycotina, Dothideales, leaf scorch, pepper spot.

Immunogold localization of callose and other plant cell wall components in soybean roots infected with the oomycete Phytophthora sojae

1997 ◽  
Vol 75 (9) ◽  
pp. 1509-1517 ◽  
Author(s):  
K. Enkerli ◽  
C. W. Mims ◽  
M. G. Hahn
Keyword(s):  
Plasma Membrane ◽  
Plant Cell Wall ◽  
Arabinogalactan Proteins ◽  
Phytophthora Sojae ◽  
Arabinogalactan Protein ◽  
Electron Microscopic ◽  
Rhamnogalacturonan I ◽  
Host Plasma Membrane ◽  
Wall Appositions ◽  
Extrahaustorial Matrix

Immunolabeling and transmission electron microscopic techniques were used to investigate the chemical nature of wall appositions in roots of susceptible and resistant soybean plants inoculated with Phytophthora sojae race 2. The extrahaustorial matrix associated with the haustorium of Phytophthora sojae also was examined. Antibodies against (1 → 3)-β-glucan, a terminal α-fucosyl-containing epitope present in xyloglucan and rhamnogalacturonan I, and an arabinosylated (1 → 6)-β-galactan epitope present in arabinogalactan proteins were used. (1 → 3)-β-Glucan (callose), xyloglucan, and arabinogalactan proteins were found to be localized in all wall appositions regardless of how long after inoculation the appositions developed or whether plants were susceptible or resistant to Phytophthora sojae. (1 → 3)-β-Glucan also was found in fungal walls and at host cell plasmodesmata. None of the four antibodies labeled the extrahaustorial matrix. The antibody against arabinogalactan protein recognized the host plasma membrane, but not the invaginated host plasma membrane associated with the extrahaustorial matrix. This result indicates that the properties or the composition of the host plasma membrane may change locally once it becomes an extrahaustorial membrane. Key words: Phytophthora sojae, Glycine max, callose, immunolabeling, wall appositions, papillae.

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.

Ultrastructure of the Host-Parasite Relationships of Pseudoperonospora humuli on Hops

1977 ◽  
Vol 25 (6) ◽  
pp. 585 ◽  
Author(s):  
RD Pares ◽  
AD Greenwood
Keyword(s):  
Leaf Tissue ◽  
Host Cells ◽  
Wall Structure ◽  
Infected Leaf ◽  
Cell Penetration ◽  
Pseudoperonospora Humuli ◽  
Host Cell Wall ◽  
Staining Techniques ◽  
Host Parasite ◽  
Infected Leaf Tissue

Infected leaf tissue was examined at 3, 4, 5 and 6 days after inoculation, after different fixing and staining techniques. One example of stomata1 penetration was seen. Examples of cell penetration and haustorium development were examined in detail. Haustoria penetrate host cells by altering host cell wall structure, and lomasomes are frequently present in the haustorium neck. Haustoria do not have nuclei and in early stages have abundant mitochondria that gradually decrease in number as infection advances.

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.

scholarly journals The autophagic machinery ensures nonlytic transmission of mycobacteria

2015 ◽  
Vol 112 (7) ◽  
pp. E687-E692 ◽  
Author(s):  
Lilli Gerstenmaier ◽  
Rachel Pilla ◽  
Lydia Herrmann ◽  
Hendrik Herrmann ◽  
Monica Prado ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Host Cell ◽  
Bacterial Pathogens ◽  
Host Cells ◽  
Phagocytic Cells ◽  
Ejection Process ◽  
Cell Transmission ◽  
Host Plasma Membrane

In contrast to mechanisms mediating uptake of intracellular bacterial pathogens, bacterial egress and cell-to-cell transmission are poorly understood. Previously, we showed that the transmission of pathogenic mycobacteria between phagocytic cells also depends on nonlytic ejection through an F-actin based structure, called the ejectosome. How the host cell maintains integrity of its plasma membrane during the ejection process was unknown. Here, we reveal an unexpected function for the autophagic machinery in nonlytic spreading of bacteria. We show that ejecting mycobacteria are escorted by a distinct polar autophagocytic vacuole. If autophagy is impaired, cell-to-cell transmission is inhibited, the host plasma membrane becomes compromised and the host cells die. These findings highlight a previously unidentified, highly ordered interaction between bacteria and the autophagic pathway and might represent the ancient way to ensure nonlytic egress of bacteria.

scholarly journals Host cell perforation by listeriolysin O (LLO) activates a Ca2+-dependent cPKC/Rac1/Arp2/3 signaling pathway that promotesListeria monocytogenesinternalization independently of membrane resealing

2018 ◽  
Vol 29 (3) ◽  
pp. 270-284 ◽  
Author(s):  
Jonathan G. T. Lam ◽  
Stephen Vadia ◽  
Sarika Pathak-Sharma ◽  
Eric McLaughlin ◽  
Xiaoli Zhang ◽  
...  
Keyword(s):  
Plasma Membrane ◽  
Host Cell ◽  
Signaling Pathway ◽  
Membrane Damage ◽  
Host Cells ◽  
Listeriolysin O ◽  
Plasma Membrane Damage ◽  
Host Plasma Membrane ◽  
Membrane Resealing

Pathogen-induced host plasma membrane damage is a recently recognized mechanism used by pathogens to promote their entry into host cells. We identified key transducers activated upon host cell perforation by the pore-forming toxin LLO to promote Listeria entry. This pathway is distinct from the pathway that reseals the toxin-perforated cell.

Two action sites of AM-toxin I produced by apple pathotype of Alternaria alternata in host cells: an ultrastructural study

1981 ◽  
Vol 59 (3) ◽  
pp. 301-310 ◽  
Author(s):  
Pyoyun Park ◽  
Syoyo Nishimura ◽  
Keisuke Kohmoto ◽  
Hiroshi Otani ◽  
Kazuyuki Tsujimoto
Keyword(s):  
Cell Wall ◽  
Plasma Membrane ◽  
Amorphous Materials ◽  
Plasma Membranes ◽  
Host Cells ◽  
Ultrastructural Changes ◽  
Electron Microscopic ◽  
Electron Microscopic Autoradiography ◽  
Moderately Resistant ◽  
Membrane Cell

The localization of primary action sites of AM-toxin I in host cells was examined by ultrastructural investigation and electron microscopic autoradiography. In susceptible apple leaves, the first effect of the toxin appeared 1 h after treatment in the plasma membranes and chloroplasts of mesophyll and vascular bundle sheath cells and in the plasma membranes of phloem and epidermal cells. Membranes and vesicles which were stained positively with a specific staining solution for grana lamellae were found in the matrix of the chloroplasts, showing that the membranous materials were derived from the disrupted grana. Cell wall lesions were formed around plasmodesmata where plasma membranes were invaginated. The invaginated sites were filled with amorphous materials from degraded cell walls, including membranes derived from plasma membranes and the desmotubules extending from plasmodesmata. The modified chloroplasts and plasma membranes were observed more often as the time after the toxin treatment was prolonged. Modified plastids were not found in the leaf cells. The other cellular membranes appeared normal even 10 h after the treatment. Resistant leaf cells were rarely affected by the toxin. Not all tissues from susceptible apples were sensitive as the toxin caused no necrosis or ultrastructural changes in petal cells. Resistant petal cells were also insensitive to the toxin, but the toxin causes necrosis and ultrastructural changes in moderately resistant petal cells in which the primary effect of the toxin appeared as plasma membrane modifications. Plastids were not affected by the toxin. These results indicate that the action sites of the toxin may be located on the plasma membrane – cell wall association in susceptible leaf cells and in moderately resistant petal cells and also on the chloroplasts of susceptible cells. The results of electron microscopic autoradiography also provided evidence that the action sites of the toxin were present on chloroplasts and the plasma membrane –cell wall association of susceptible leaf cells.

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.

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