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 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.

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.

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.

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.

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.

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.

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.

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.

The Alternaria brassicae – Nectria inventa host–parasite interface

1977 ◽  
Vol 55 (4) ◽  
pp. 448-454 ◽  
Author(s):  
A. Tsuneda ◽  
W. P. Skoropad
Keyword(s):  
Cell Wall ◽  
Host Cell ◽  
Host Cells ◽  
Alternaria Brassicae ◽  
Adhesive Material ◽  
Large Hole ◽  
Mature Conidium ◽  
Host Cell Wall ◽  
Host Parasite

The Verticillium state of Nectria inventa is a destructive parasite of Alternaria brassicae. Tropic growth of parasite hyphae towards hyphae and conidia of A. brassicae occurs in the vicinity of the host. Upon contact, the parasite hyphae often form appressorium-like bodies on the host cells and produce fibrous adhesive material at the host–parasite interface. Conidia are penetrated more commonly than hyphae. Penetration of the septa in hyphae results in a separation of cells. Penetration of a mature conidium also occurs commonly at a septum. The presence of a large hole in the wall of the host cell and the meshwork of material at the penetration site suggest that enzymatic breakdown of host cell wall occurs. Juvenile conidia are penetrated usually at the basal pore.

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