An ultrastructural study of the marine diatom Licmophora hyalina and its parasite Ectrogella perforans. II. Development of the fungus in its host

1980 ◽  
Vol 58 (24) ◽  
pp. 2557-2574 ◽  
Author(s):  
Chandralata Raghu Kumar
Keyword(s):  
Plasma Membrane ◽  
Host Cell ◽  
Ultrastructural Study ◽  
Typical Feature ◽  
Golgi Body ◽  
Marine Diatom ◽  
Host Plasma Membrane ◽  
Cytoplasmic Bridges ◽  
Dense Vesicles

The thallus of the fungus Ectrogella perforans Petersen inside its host, the diatom Licmophora hyalina Agardh, is surrounded initially by two electron-dense membranes, of which the outer one is the invaginated host plasma membrane and the inner one, the fungal plasma membrane. Later, new membranes are added between these two membranes and the fungal envelope consists of four to six membranes. When the fungal thallus is mature, all the membranes except the fungal plasmalemma break down and it secretes an amorphous wall around itself. This coincides with the breakdown of host organelles followed by death of the host cell. Zoosporogenesis begins after the sporangium becomes multinucleate. A peculiar "multitubular body" is always observed in the multinucleate sporangium. A typical feature of the multinucleate sporangium prior to zoosporogenesis is the presence of a ring of tubular cisternae around the nuclei, electron-dense vesicles, and granular vesicles.The tubular cisternae found around the nuclei move away and act as cleavage cisternae. The cleavage cisternae run perpendicular to the sporangial plasma membrane and delimit the sporangial mass into uninucleate units at the time of zoosporogenesis. Simultaneously, vesicles are pinched off from the Golgi body which act as cleavage vesicles. These cleavage vesicles fuse with each other and form cleavage furrows. The cleavage cisternae fuse with the plasma membrane outside and with the cleavage vesicles inside and thus deepen the cleavage furrows. The sporangial mass is thus divided into zoospore units and the units are connected only by narrow cytoplasmic bridges. The zoospores have their flagella developed already. The structure of primary zoospores, encysted primary zoospores, and encysted secondary zoospores is described here.

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.

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.

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.

scholarly journals Role of Predicted Transmembrane Domains for Type III Translocation, Pore Formation, and Signaling by the Yersinia pseudotuberculosis YopB Protein

2005 ◽  
Vol 73 (4) ◽  
pp. 2433-2443 ◽  
Author(s):  
Michelle B. Ryndak ◽  
Hachung Chung ◽  
Erwin London ◽  
James B. Bliska
Keyword(s):  
Plasma Membrane ◽  
Cell Signaling ◽  
Host Cell ◽  
Pore Formation ◽  
Yersinia Pseudotuberculosis ◽  
Transmembrane Domain ◽  
Membrane Insertion ◽  
Type Iii ◽  
Host Cell Signaling ◽  
Host Plasma Membrane

ABSTRACT YopB is a 401-amino-acid protein that is secreted by a plasmid-encoded type III secretion system in pathogenic Yersinia species. YopB is required for Yersinia spp. to translocate across the host plasma membrane a set of secreted effector proteins that function to counteract immune signaling responses and to induce apoptosis. YopB contains two predicted transmembrane helices (residues 166 to 188 and 228 to 250) that are thought to insert into the host plasma membrane during translocation. YopB is also required for pore formation and host-cell-signaling responses to the type III machinery, and these functions of YopB may also require membrane insertion. To elucidate the importance of membrane insertion for YopB function, YopB proteins containing helix-disrupting double consecutive proline substitutions in the center of each transmembrane domain were constructed. Yersinia pseudotuberculosis strains expressing the mutant YopB proteins were used to infect macrophages or epithelial cells. Effector translocation, pore formation, and host-cell-signaling responses were studied. Introduction of helix-disrupting substitutions into the second transmembrane domain of YopB resulted in a nonfunctional protein that was not secreted by the type III machinery. Introduction of helix-disrupting substitutions into the first transmembrane domain of YopB resulted in a protein that was fully functional for secretion and for interaction with YopD, another component of the translocation machinery. However, the YopB protein with helix-disrupting substitutions in the first transmembrane domain was partially defective for translocation, pore formation, and signaling, suggesting that all three functions of YopB involve insertion into host membrane.

scholarly journals Host but Not Parasite Cholesterol ControlsToxoplasmaCell Entry by Modulating Organelle Discharge

2003 ◽  
Vol 14 (9) ◽  
pp. 3804-3820 ◽  
Author(s):  
Isabelle Coppens ◽  
Keith A. Joiner
Keyword(s):  
Plasma Membrane ◽  
Host Cell ◽  
Parasitophorous Vacuole ◽  
Protozoan Parasite ◽  
Inhibitory Effect ◽  
Microbial Pathogens ◽  
Membrane Cholesterol ◽  
Cell Plasma ◽  
Host Plasma Membrane ◽  
Plasma Membrane Cholesterol

Host cell cholesterol is implicated in the entry and replication of an increasing number of intracellular microbial pathogens. Although uptake of viral particles via cholesterol-enriched caveolae is increasingly well described, the requirement of cholesterol for internalization of eukaryotic pathogens is poorly understood and is likely to be partly organism specific. We examined the role of cholesterol in active host cell invasion by the protozoan parasite Toxoplasma gondii. The parasitophorous vacuole membrane (PVM) surrounding T. gondii contains cholesterol at the time of invasion. Although cholesterol-enriched parasite apical organelles termed rhoptries discharge at the time of cell entry and contribute to PVM formation, surprisingly, rhoptry cholesterol is not necessary for this process. In contrast, host plasma membrane cholesterol is incorporated into the forming PVM during invasion, through a caveolae-independent mechanism. Unexpectedly, depleting host cell plasma membrane cholesterol blocks parasite internalization by reducing the release of rhoptry proteins that are necessary for invasion. Cholesterol back-addition into host plasma membrane reverses this inhibitory effect of depletion on parasite secretion. These data define a new mechanism by which host cholesterol specifically controls entry of an intracellular 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.

scholarly journals The Gb3-enriched CD59/flotillin plasma membrane domain regulates host cell invasion by Pseudomonas aeruginosa

2021 ◽  
Author(s):  
Annette Brandel ◽  
Sahaja Aigal ◽  
Simon Lagies ◽  
Manuel Schlimpert ◽  
Ana Valeria Meléndez ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Plasma Membrane ◽  
Host Cell ◽  
Acyl Chain ◽  
Mass Spectrometry Analysis ◽  
Bacterial Invasion ◽  
Fatty Acyl Chain ◽  
Membrane Domain ◽  
Host Cell Membrane ◽  
Plasma Membrane Domain

AbstractThe opportunistic pathogen Pseudomonas aeruginosa has gained precedence over the years due to its ability to develop resistance to existing antibiotics, thereby necessitating alternative strategies to understand and combat the bacterium. Our previous work identified the interaction between the bacterial lectin LecA and its host cell glycosphingolipid receptor globotriaosylceramide (Gb3) as a crucial step for the engulfment of P. aeruginosa via the lipid zipper mechanism. In this study, we define the LecA-associated host cell membrane domain by pull-down and mass spectrometry analysis. We unraveled a predilection of LecA for binding to saturated, long fatty acyl chain-containing Gb3 species in the extracellular membrane leaflet and an induction of dynamic phosphatidylinositol (3,4,5)-trisphosphate (PIP3) clusters at the intracellular leaflet co-localizing with sites of LecA binding. We found flotillins and the GPI-anchored protein CD59 not only to be an integral part of the LecA-interacting membrane domain, but also majorly influencing bacterial invasion as depletion of either of these host cell proteins resulted in about 50% reduced invasiveness of the P. aeruginosa strain PAO1. In summary, we report that the LecA-Gb3 interaction at the extracellular leaflet induces the formation of a plasma membrane domain enriched in saturated Gb3 species, CD59, PIP3 and flotillin thereby facilitating efficient uptake of PAO1.

scholarly journals Three in one: evolution of viviparity, coenocytic placenta and polyembryony in cyclostome bryozoans

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
U. A. Nekliudova ◽  
T. F. Schwaha ◽  
O. N. Kotenko ◽  
D. Gruber ◽  
N. Cyran ◽  
...  
Keyword(s):  
Ultrastructural Study ◽  
Main Part ◽  
Structural Diversity ◽  
Early Embryo ◽  
Unique Combination ◽  
Nutritive Tissue ◽  
Pore Cells ◽  
Secondary Embryos ◽  
Cytoplasmic Bridges ◽  
Hydrostatic System

Abstract Background Placentation has evolved multiple times among both chordates and invertebrates. Although they are structurally less complex, invertebrate placentae are much more diverse in their origin, development and position. Aquatic colonial suspension-feeders from the phylum Bryozoa acquired placental analogues multiple times, representing an outstanding example of their structural diversity and evolution. Among them, the clade Cyclostomata is the only one in which placentation is associated with viviparity and polyembryony—a unique combination not present in any other invertebrate group. Results The histological and ultrastructural study of the sexual polymorphic zooids (gonozooids) in two cyclostome species, Crisia eburnea and Crisiella producta, revealed embryos embedded in a placental analogue (nutritive tissue) with a unique structure—comprising coenocytes and solitary cells—previously unknown in animals. Coenocytes originate via nuclear multiplication and cytoplasmic growth among the cells surrounding the early embryo. This process also affects cells of the membranous sac, which initially serves as a hydrostatic system but later becomes main part of the placenta. The nutritive tissue is both highly dynamic, permanently rearranging its structure, and highly integrated with its coenocytic ‘elements’ being interconnected via cytoplasmic bridges and various cell contacts. This tissue shows evidence of both nutrient synthesis and transport (bidirectional transcytosis), supporting the enclosed multiple progeny. Growing primary embryo produces secondary embryos (via fission) that develop into larvae; both the secondary embyos and larvae show signs of endocytosis. Interzooidal communication pores are occupied by 1‒2 specialized pore-cells probably involved in the transport of nutrients between zooids. Conclusions Cyclostome nutritive tissue is currently the only known example of a coenocytic placental analogue, although syncytial ‘elements’ could potentially be formed in them too. Structurally and functionally (but not developmentally) the nutritive tissue can be compared with the syncytial placental analogues of certain invertebrates and chordates. Evolution of the cyclostome placenta, involving transformation of the hydrostatic apparatus (membranous sac) and change of its function to embryonic nourishment, is an example of exaptation that is rather widespread among matrotrophic bryozoans. We speculate that the acquisition of a highly advanced placenta providing massive nourishment might support the evolution of polyembryony in cyclostomes. In turn, massive and continuous embryonic production led to the evolution of enlarged incubating polymorphic gonozooids hosting multiple progeny.

Sign in / Sign up

Export Citation Format

Share Document