scholarly journals Early events in living epidermal cells of cowpea and broad bean during infection with basidiospores of the cowpea rust fungus

1991 ◽  
Vol 69 (10) ◽  
pp. 2279-2285 ◽  
Author(s):  
Haixin Xu ◽  
Kurt Mendgen
Keyword(s):  
Vicia Faba ◽  
Broad Bean ◽  
Rust Fungus ◽  
Infection Process ◽  
Host Cells ◽  
Appressorium Formation ◽  
Vigna Sinensis ◽  
Infected Cells ◽  
Uromyces Vignae ◽  
Defence Reactions

The infection process of basidiospores of the cowpea rust fungus (Uromyces vignae) was studied on living host (Vigna sinensis) and nonhost (Vicia faba) leaves using light microscopy with differential interference contrast optics. During the first 8 h, fungal development was similar on host and on nonhost leaves. Penetration and production of intraepidermal vesicles occurred in nonhost cells 4 h earlier than in host cells. Penetration frequency was also higher in nonhost leaves. These results suggest that the cuticle of the cowpea plant delays basidiospore infection. Both host and nonhost cells produced cytoplasmic aggregates during appressorium formation and again, a few hours later, during penetration of the epidermal cell wall. Cytoplasmic aggregates were also observed in cells adjacent to a collapsing cell. Papillae were observed at most infection sites in both host and nonhost cells. The nuclei of infected cells migrated towards the penetration site in both plant–pathogen combinations. Nuclear size increased considerably only in the nonhost epidermis and decreased again markedly after cell collapse. In the nonhost cells, three types of defence reactions occurred during or after formation of the intraepidermal vesicle. First, following the halt of cytoplasmic streaming, the cytoplasm of the invaded cell either contracted or disintegrated into granules. Alternatively, the cytoplasm continued streaming but darkly pigmented material encased the fungal infection structure. Key words: basidiospore, broad bean (Vicia faba), cowpea (Vigna sinensis), cowpea rust fungus (Uromyces vignae), hypersensitivity, nonhost resistance.

Ultrastructure of eastern cottonwood clones susceptible or resistant to leaf rust

1987 ◽  
Vol 65 (8) ◽  
pp. 1586-1598 ◽  
Author(s):  
L. Shain ◽  
U. Järlfors
Keyword(s):  
Electron Microscopy ◽  
Leaf Rust ◽  
Light And Electron Microscopy ◽  
Infection Process ◽  
The Other ◽  
Host Cells ◽  
Eastern Cottonwood ◽  
Melampsora Medusae ◽  
Wall Appositions ◽  
Infected Cells

The infection process in four clones of eastern cottonwood susceptible or resistant to leaf rust caused by Melampsora medusae was studied by light and electron microscopy. Infection was initiated by stomatal rather than direct entry. Typical dikaryotic haustoria were observed in all clones within 1 day of inoculation. Some healthy-appearing haustoria were observed in susceptible clones throughout the duration of the study, which was terminated during the initiation of uredial production. Incompatibility was expressed differently in the two resistant clones. In clone St 75, most haustoria and invaded host cells that were observed appeared necrotic within 2 days of inoculation. Cell wall appositions appeared during this time in cells adjoining necrotic host cells. Some infected cells disintegrated within 4 days of inoculation. Affected host cells of clone St 92, on the other hand, plasmolyzed during the first 2 to 3 days after inoculation. Necrotic host cells were not observed in this clone until the 4th day after inoculation. Hyphal ramification and host plasmolysis were extensive at 6 days after inoculation.

Effects of environment on spore germination and infection by broad bean rust (Uromyces viciae-fabae)

1997 ◽  
Vol 128 (1) ◽  
pp. 73-78 ◽  
Author(s):  
M. E. JOSEPH ◽  
T. F. HERING
Keyword(s):  
Vicia Faba ◽  
Spore Germination ◽  
Broad Bean ◽  
Infection Process ◽  
Leaf Wetness ◽  
Artificial Light ◽  
Light Sources ◽  
Bean Rust ◽  
Light Intensities

Urediospores of U. viciae-fabae (broad bean rust) germinated well in the range 5–26 °C, with fastest germination at 20 °C. Exposure to 30 °C gave poor germination and damaged the spores. Infection of Vicia faba leaves depended on a moisture film. At 20 °C some infection occurred with only 4 h leaf wetness, but longer wet periods up to 24 h gave increased infection. At lower temperatures, the infection process was slower and final pustule numbers were smaller. Spore germination was delayed by daylight and by all artificial light sources that contained far-red (700–800 nm) wavelengths. The delay was increased at higher light intensities. When spores were subjected to alternating periods of light and darkness, it was found that 40 min of darkness was sufficient for the irreversible induction of germination at 20 °C.

scholarly journals Characterization of a novel NADP+-dependent D-arabitol dehydrogenase from the plant pathogen Uromyces fabae

2005 ◽  
Vol 389 (2) ◽  
pp. 289-295 ◽  
Author(s):  
Tobias Link ◽  
Gertrud Lohaus ◽  
Ingrid Heiser ◽  
Kurt Mendgen ◽  
Matthias Hahn ◽  
...  
Keyword(s):  
Plant Pathogen ◽  
Broad Bean ◽  
Rust Fungus ◽  
Plant Defence ◽  
In Vitro System ◽  
Uromyces Fabae ◽  
Factor Specificity ◽  
Defence Reactions

We have identified and characterized a novel NADP+-dependent D-arabitol dehydrogenase and the corresponding gene from the rust fungus Uromyces fabae, a biotrophic plant pathogen on broad bean (Vicia faba). The new enzyme was termed ARD1p (D-arabitol dehydrogenase 1). It recognizes D-arabitol and mannitol as substrates in the forward reaction, and D-xylulose, D-ribulose and D-fructose as substrates in the reverse reaction. Co-factor specificity was restricted to NADP(H). Kinetic data for the major substrates and co-factors are presented. A detailed analysis of the organization and expression pattern of the ARD1 gene are also given. Immunocytological data indicate a localization of the gene product predominantly in haustoria, the feeding structures of these fungi. Analyses of metabolite levels during pathogenesis indicate that the D-arabitol concentration rises dramatically as infection progresses, and D-arabitol was shown in an in vitro system to be capable of quenching reactive oxygen species involved in host plant defence reactions. ARD1p may therefore play an important role in carbohydrate metabolism and in establishing and/or maintaining the biotrophic interaction in U. fabae.

scholarly journals Differentiation of aecidiospore- and uredospore-derived infection structures on cowpea leaves and on artificial surfaces by Uromyces vignae

1993 ◽  
Vol 71 (9) ◽  
pp. 1236-1242 ◽  
Author(s):  
M. Stark-Urnau ◽  
K. Mendgen
Keyword(s):  
Key Words ◽  
Mother Cell ◽  
Host Plants ◽  
Rust Fungus ◽  
Host Cells ◽  
In Planta ◽  
Infection Structures ◽  
Artificial Surfaces ◽  
Uromyces Vignae ◽  
Mother Cells

Aecidiospores and uredospores are the two dikaryotic spore forms of the cowpea rust fungus Uromyces vignae. After germination they can be induced to develop a series of infection structures including appressoria, infection hyphae, and haustorial mother cells. Haustoria are then formed within host cells. The differentiation of infection structures was compared on polystyrene membranes with defined topographies, on scratched polyethylene membranes, and in planta. On polystyrene membranes with defined topographies both sporelings showed highest rates of differentiation on ridges 0.3 μm high but aecidiosporelings responded less efficiently to this stimulus than uredosporelings. On scratched polyethylene membranes, almost 90% of both sporelings differentiated appressoria, but only 10% formed haustorial mother cells; haustoria were not observed. On the host plant, by contrast, only 50% of the sporelings differentiated appressoria, but most of these formed haustorial mother cells and haustoria. In planta haustorial mother cell development occurred approximately 6 h earlier than on inductive membranes. Infection structures formed on artificial membranes and on host plants were similar in morphology and nuclear condition. Key words: cowpea rust fungus, nucleus, appressorium.

Changes in actin microfilament arrays in developing pea root nodule cells

2001 ◽  
Vol 79 (7) ◽  
pp. 767-776 ◽  
Author(s):  
A L Davidson ◽  
W Newcomb
Keyword(s):  
Rhizobium Leguminosarum ◽  
Root Nodule ◽  
Infection Process ◽  
Host Cells ◽  
Actin Microfilaments ◽  
Symbiotic Associations ◽  
Actin Microfilament ◽  
Pea Root ◽  
Microfilament Bundles ◽  
Infected Cells

Various microorganisms that form symbiotic associations with plant roots alter the cytoskeleton of host cells. The objective of this study was to determine the organization of actin microfilaments in developing Pisum sativum L. (pea) root nodule cells at various stages after infection by Rhizobium leguminosarum bv. viciae. Fluorescently labelled microfilaments in uninfected pea root nodule cells occur in association with the nucleus, along cytoplasmic strands, and as long microfilament bundles randomly organized in the cortex of the cell. These actin arrays are also present in recently infected cells that have been invaded by an infection thread and contain a small number of bacteroids. In addition, the recently infected cells contain diffuse cytoplasmic actin, long actin microfilament bundles near the vacuole, and a nuclear-associated network of microfilament bundles. In older infected cells, the predominant array is a network of cytoplasmic microfilaments that are wavy and extend in multiple directions within the cell; the network is equally abundant in all regions of the cytoplasm and may interact with the bacteroids and organelles. Thus, actin microfilaments reorganize during the pea root nodule infection process to form distinct arrays whose organization depends on the stage of infection.Key words: nodule, actin microfilaments, Rhizobium, pea, symbiosis.

scholarly journals Helicobacter pylori Outer Membrane Vesicles and Extracellular Vesicles from Helicobacter pylori-Infected Cells in Gastric Disease Development

2021 ◽  
Vol 22 (9) ◽  
pp. 4823
Author(s):  
María Fernanda González ◽  
Paula Díaz ◽  
Alejandra Sandoval-Bórquez ◽  
Daniela Herrera ◽  
Andrew F. G. Quest
Keyword(s):  
Gastric Cancer ◽  
Helicobacter Pylori ◽  
Outer Membrane ◽  
Extracellular Vesicles ◽  
Membrane Vesicles ◽  
Outer Membrane Vesicles ◽  
Host Cells ◽  
Gastric Epithelium ◽  
Infected Cells ◽  
H Pylori

Extracellular vesicles (EVs) are cell-derived vesicles important in intercellular communication that play an essential role in host-pathogen interactions, spreading pathogen-derived as well as host-derived molecules during infection. Pathogens can induce changes in the composition of EVs derived from the infected cells and use them to manipulate their microenvironment and, for instance, modulate innate and adaptive inflammatory immune responses, both in a stimulatory or suppressive manner. Gastric cancer is one of the leading causes of cancer-related deaths worldwide and infection with Helicobacter pylori (H. pylori) is considered the main risk factor for developing this disease, which is characterized by a strong inflammatory component. EVs released by host cells infected with H. pylori contribute significantly to inflammation, and in doing so promote the development of disease. Additionally, H. pylori liberates vesicles, called outer membrane vesicles (H. pylori-OMVs), which contribute to atrophia and cell transformation in the gastric epithelium. In this review, the participation of both EVs from cells infected with H. pylori and H. pylori-OMVs associated with the development of gastric cancer will be discussed. By deciphering which functions of these external vesicles during H. pylori infection benefit the host or the pathogen, novel treatment strategies may become available to prevent disease.

scholarly journals “Limiting access to iron decreases infection of Atlantic salmon SHK-1 cells with bacterium Piscirickettsia salmonis”

2021 ◽  
Vol 17 (1) ◽  
Author(s):  
Rodrigo Díaz ◽  
José Troncoso ◽  
Eva Jakob ◽  
Stanko Skugor
Keyword(s):  
Gene Expression ◽  
Iron Deficiency ◽  
Atlantic Salmon ◽  
Bacterial Load ◽  
Host Cells ◽  
Immune Gene ◽  
Immune Signaling ◽  
Immune Effector ◽  
Infected Cells ◽  
Piscirickettsia Salmonis

Abstract Background Vertebrate hosts limit the availability of iron to microbial pathogens in order to nutritionally starve the invaders. The impact of iron deficiency induced by the iron chelator deferoxamine mesylate (DFO) was investigated in Atlantic salmon SHK-1 cells infected with the facultative intracellular bacterium Piscirickettsia salmonis. Results Effects of the DFO treatment and P. salmonis on SHK-1 cells were gaged by assessing cytopathic effects, bacterial load and activity, and gene expression profiles of eight immune biomarkers at 4- and 7-days post infection (dpi) in the control group, groups receiving single treatments (DFO or P. salmonis) and their combination. The chelator appears to be well-tolerated by host cells, while it had a negative impact on the number of bacterial cells and associated cytotoxicity. DFO alone had minor effects on gene expression of SHK-1 cells, including an early activation of IL-1β at 4 dpi. In contrast to few moderate changes induced by single treatments (either infection or chelator), most genes had highest upregulation in the infected groups receiving DFO. The mildest induction of hepcidin-1 (antimicrobial peptide precursor and regulator of iron homeostasis) was observed in cells exposed to DFO alone, followed by P. salmonis infected cells while the addition of DFO to infected cells further increased the mRNA abundance of this gene. Transcripts encoding TNF-α (immune signaling) and iNOS (immune effector) showed sustained increase at both time points in this group while cathelicidin-1 (immune effector) and IL-8 (immune signaling) were upregulated at 7 dpi. The stimulation of protective gene responses seen in infected cultures supplemented with DFO coincided with the reduction of bacterial load and activity (judged by the expression of P. salmonis 16S rRNA), and damage to cultured host cells. Conclusion The absence of immune gene activation under normal iron conditions suggests modulation of host responses by P. salmonis. The negative effect of iron deficiency on bacteria likely allowed host cells to respond in a more protective manner to the infection, further decreasing its progression. Presented findings encourage in vivo exploration of iron chelators as a promising strategy against piscirickettsiosis.

scholarly journals Revisiting Ehrlichia ruminantium Replication Cycle Using Proteomics: The Host and the Bacterium Perspectives

2021 ◽  
Vol 9 (6) ◽  
pp. 1144
Author(s):  
Isabel Marcelino ◽  
Philippe Holzmuller ◽  
Ana Coelho ◽  
Gabriel Mazzucchelli ◽  
Bernard Fernandez ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Host Cell ◽  
Cell Metabolism ◽  
Replication Cycle ◽  
Host Cells ◽  
Ehrlichia Ruminantium ◽  
Host Interaction ◽  
Infected Cells ◽  
Related Proteins

The Rickettsiales Ehrlichia ruminantium, the causal agent of the fatal tick-borne disease Heartwater, induces severe damage to the vascular endothelium in ruminants. Nevertheless, E. ruminantium-induced pathobiology remains largely unknown. Our work paves the way for understanding this phenomenon by using quantitative proteomic analyses (2D-DIGE-MS/MS, 1DE-nanoLC-MS/MS and biotin-nanoUPLC-MS/MS) of host bovine aorta endothelial cells (BAE) during the in vitro bacterium intracellular replication cycle. We detect 265 bacterial proteins (including virulence factors), at all time-points of the E. ruminantium replication cycle, highlighting a dynamic bacterium–host interaction. We show that E. ruminantium infection modulates the expression of 433 host proteins: 98 being over-expressed, 161 under-expressed, 140 detected only in infected BAE cells and 34 exclusively detected in non-infected cells. Cystoscape integrated data analysis shows that these proteins lead to major changes in host cell immune responses, host cell metabolism and vesicle trafficking, with a clear involvement of inflammation-related proteins in this process. Our findings led to the first model of E. ruminantium infection in host cells in vitro, and we highlight potential biomarkers of E. ruminantium infection in endothelial cells (such as ROCK1, TMEM16K, Albumin and PTPN1), which may be important to further combat Heartwater, namely by developing non-antibiotic-based strategies.

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