The effect of the Sr6 gene for host resistance on histological events during the development of stem rust in near-isogenic wheat lines

1974 ◽  
Vol 52 (5) ◽  
pp. 1107-1115 ◽  
Author(s):  
R. A. Skipp ◽  
D. J. Samborski
Keyword(s):  
Host Cell ◽  
Host Resistance ◽  
Infection Type ◽  
Fungal Growth ◽  
Host Cells ◽  
Puccinia Graminis ◽  
Cell Necrosis ◽  
Resistant Line ◽  
Resistant Infection ◽  
Wheat Lines

Seedling leaves of resistant (Sr6) and susceptible (sr6) near-isogenic wheat lines inoculated with urediospores of Puccinia graminis f. sp. tritici race C 17 (56) became infected at similar rates. Host cells of the resistant line became necrotic after haustorial penetration (beginning about 20 h after inoculation), whereas necrosis was rarely seen in the susceptible line and colonies grew to form sporulating pustules. Some colonies in the resistant line appeared to have stopped growing by about 60 h after inoculation, while others grew slowly, the area of necrosis increasing as they expanded.Inoculated resistant-line plants became susceptible when incubated at 25 °C rather than 20 °C. Provided that the plants were kept at 25 °C for at least 1 day before inoculation, no host cell became necrotic. The necrotic response was resumed, and a more resistant infection type developed when infected seedlings were transferred from 25 °C to 20 °C. The converse occurred when resistant plants were grown and incubated at 20 °C, then transferred to 25 °C.Effects on fungal growth and the action of the Sr6 gene were considered to be closely associated with host cell necrosis. Temperature sensitivity appeared to be a property of the host plant.

Effect of blasticidin S, ethionine, and polyoxin D on stem rust development and host-cell necrosis in wheat near-isogenic for gene Sr6

1977 ◽  
Vol 55 (5) ◽  
pp. 568-573 ◽  
Author(s):  
W. K. Kim ◽  
R. Rohringer ◽  
D. J. Samborski ◽  
N. K. Howes
Keyword(s):  
Host Cell ◽  
Stem Rust ◽  
Fungal Growth ◽  
Triticum Aestivum L ◽  
Hypersensitive Reaction ◽  
Host Cells ◽  
Puccinia Graminis ◽  
Cell Necrosis ◽  
Blasticidin S ◽  
Wheat Leaves

Seedlings of resistant (Sr6) and susceptible (sr6) near-isogenic lines of wheat (Triticum aestivum L.) were inoculated with an avirulent (P6) race of stem rust (Puccinia graminis (Pers.) f.sp. tritici Eriks. & Henn.) and kept for 2 days at 26 °C where the Sr6 gene is ineffective, treated with blasticidin S, ethionine, polyoxin D, or buffer, and transferred to 19 °C where the Sr6 gene is normally effective. One and 2 days later, leaves were stained with Calcofluor and examined by fluorescence microscopy to detect autofluorescing necrotic host cells and Calcofluor-stained stem rust colonies.Blasticidin S was phytotoxic to wheat leaves at concentrations that had no effect on fungal growth during the first 2 days after treatment. At later stages, extensive host necrosis, resulting from the phytotoxicity of this antibiotic, inhibited rust development.Ethionine and polyoxin D strongly inhibited rust development at concentrations that were not phytotoxic. In genotypically resistant leaves treated with ethionine and polyoxin D there were fewer necrotic cells associated with stem rust colonies than in leaves treated with buffer. The spacial distribution of necrotic cells was consistent with the view that necrosis occurs only in cells newly invaded after the temperature was lowered to 19 °C.The observations do not support the concept that host-cell necrosis in the hypersensitive reaction conditioned by this gene results from the death of the fungus.

Histological studies on host-cell necrosis conditioned by the Sr6 gene for resistance in wheat to stem rust

1977 ◽  
Vol 55 (11) ◽  
pp. 1445-1452 ◽  
Author(s):  
D. J. Samborski ◽  
W. K. Kim ◽  
R. Rohringer ◽  
N. K. Howes ◽  
R. J. Baker
Keyword(s):  
Triticum Aestivum ◽  
Stem Rust ◽  
Fungal Growth ◽  
Triticum Aestivum L ◽  
Host Cells ◽  
Puccinia Graminis ◽  
Near Isogenic Lines ◽  
Cell Necrosis ◽  
Calcofluor White ◽  
Histological Studies

Seedlings of resistant (Sr6) and susceptible (sr6) near-isogenic lines of wheat (Triticum aestivum L.) were inoculated with a race of stem rust (Puccinia graminis Pers. f. sp. tritici Eriks. & E. Henn.) that was avirulent on the line with Sr6 and they were kept at 19, 25, 26, and 27 °C. Fluorescence microscopy was used to detect autofluorescing necrotic host cells and rust colonies after these were stained with a fiuorochrome (Calcofluor White M2R New).In leaves containing the Sr6 gene, a smaller percentage of colonies grown at 25 °C had necrotic cells associated with them than those that were grown at 19 °C. The incidence of colony-associated necrosis in these leaves could be further reduced by increasing the temperature to 26 °C and 27 °C. Similarly, the number of necrotic host cells per colony decreased with an increase in temperature. Colonies in genotypically resistant leaves were usually smaller than those in genotypically susceptible leaves, but the differences in colony sizes between these two lines decreased at the higher temperatures.When infected plants containing the Sr6 gene were kept for varying times at 25 °C and then were transferred to 19 °C, there was significantly less fungal growth and more necrosis than in plants kept continuously at 25 °C. This necrosis occurred largely in those cells that were invaded after the transfer to 19 °C, when the Sr6 gene was activated.

Lomasomes in wheat leaves infected by Puccinia graminis and P. recondita

1968 ◽  
Vol 46 (1) ◽  
pp. 17-20 ◽  
Author(s):  
Mary A. Ehrlich ◽  
John F. Schafer ◽  
Howard G. Ehrlich
Keyword(s):  
Cell Wall ◽  
Host Resistance ◽  
Mesophyll Cell ◽  
Host Cells ◽  
Puccinia Graminis ◽  
Mesophyll Cells ◽  
Dark Staining ◽  
Dark Material ◽  
Wheat Leaves ◽  
Type Infection

Boundary formations (lomasomes) have been observed between the plasmalemma and wall of mesophyll cells in Puccinia graminis and P. recondita infected wheat plants. They were present in host cells from both resistant- and susceptible-type infection centers, and were especially frequent and massive in plants grown at low (65–70 °F) temperatures. They appeared to occur in response to the presence of the pathogen, but did not seem to be associated with either host resistance or susceptibility. The dark-staining masses present in the lomasomes were often dense and extremely irregular in shape, but some of the dark material occasionally appeared vesicular or tubular. The suggestion is made that the lomasomes observed in the present investigation may be associated with infection-induced alterations in the mesophyll cell wall.

scholarly journals The Functional Characterization of Podosphaera xanthii Candidate Effector Genes Reveals Novel Target Functions for Fungal Pathogenicity

2018 ◽  
Vol 31 (9) ◽  
pp. 914-931 ◽  
Author(s):  
Jesús Martínez-Cruz ◽  
Diego Romero ◽  
Fernando N. de la Torre ◽  
Dolores Fernández-Ortuño ◽  
Juan A. Torés ◽  
...  
Keyword(s):  
Host Cell ◽  
Binding Protein ◽  
Functional Characterization ◽  
Fungal Growth ◽  
Phytopathogenic Fungi ◽  
Host Cells ◽  
Podosphaera Xanthii ◽  
Production Of Hydrogen ◽  
Predicted Signal Peptide ◽  
Novel Target

Podosphaera xanthii is the main causal agent of powdery mildew disease in cucurbits. In a previous study, we determined that P. xanthii expresses approximately 50 Podosphaera effector candidates (PECs), identified based on the presence of a predicted signal peptide and the absence of functional annotation. In this work, we used host-induced gene silencing (HIGS), employing Agrobacterium tumefaciens as a vector for the delivery of the silencing constructs (ATM-HIGS), to identify genes involved in early plant-pathogen interaction. The analysis of seven selected PEC-encoding genes showed that six of them, PEC007, PEC009, PEC019, PEC032, PEC034, and PEC054, are required for P. xanthii pathogenesis, as revealed by reduced fungal growth and increased production of hydrogen peroxide by host cells. In addition, protein models and protein-ligand predictions allowed us to identify putative functions for these candidates. The biochemical activities of PEC019, PEC032, and PEC054 were elucidated using their corresponding proteins expressed in Escherichia coli. These proteins were confirmed as phospholipid-binding protein, α-mannosidase, and cellulose-binding protein. Further, BLAST searches showed that these three effectors are widely distributed in phytopathogenic fungi. These results suggest novel targets for fungal effectors, such as host-cell plasma membrane, host-cell glycosylation, and damage-associated molecular pattern–triggered immunity.

Electron microscopy studies on infection of resistant (Sr6 gene) and susceptible near-isogenic wheat lines by Puccinia graminis f. sp. tritici

1974 ◽  
Vol 52 (12) ◽  
pp. 2615-2620 ◽  
Author(s):  
R. A. Skipp ◽  
D. E. Harder ◽  
D. J. Samborski
Keyword(s):  
Electron Microscopy ◽  
Fungal Growth ◽  
Host Cells ◽  
Wheat Line ◽  
Mesophyll Cells ◽  
Susceptible Line ◽  
Infected Cells ◽  
Mother Cells ◽  
Wheat Lines ◽  
Infection Hypha

Intracellular hyphae, haustoria, and infected host cells in young stem rust infections of a wheat line containing resistance gene Sr6 were compared by electron microscopy with those of a near-isogenic susceptible line. Mesophyll cells of the resistant line which had undergone a rapid necrotic response to haustorial invasion were collapsed and lacked the thin layer of cytoplasm that typically bounded the vacuole of infected cells of the susceptible line. Instead, the lumen was filled with an electron-dense ground material of mixed cytoplasmic and vacuolar constituents containing organelles at various stages of disorganization. Haustoria within these cells were necrotic, as were their mother cells. Apart from a dense staining of mitochondrial membranes there was little evidence of damage to the infection hypha proximal to the septum of the haustorium mother cell. The cytoplasm of host cells adjacent to those showing necrosis was often diffuse and vesiculated. A deposit of electron-dense granular material was found between the wall of a necrotic cell and its plasmalemma, and a similar deposit was present inside the adjoining wall of a contiguous non-necrotic cell.These findings are discussed in relation to the inhibition of fungal growth that accompanies host cell necrosis in the resistant wheat line.

scholarly journals Detection of Virulence to Resistance Gene Sr24 Within Race TTKS of Puccinia graminis f. sp. tritici

Plant Disease ◽  
2008 ◽  
Vol 92 (6) ◽  
pp. 923-926 ◽  
Author(s):  
Y. Jin ◽  
L. J. Szabo ◽  
Z. A. Pretorius ◽  
R. P. Singh ◽  
R. Ward ◽  
...  
Keyword(s):  
Resistance Gene ◽  
North American ◽  
Stem Rust ◽  
Infection Type ◽  
Genetic Lineage ◽  
Puccinia Graminis ◽  
The North ◽  
New Variant ◽  
Group B ◽  
Wheat Lines

The stem rust resistance gene Sr24 is effective against most races of Puccinia graminis f. sp. tritici, including race TTKS (syn. Ug99), and is used widely in commercial wheat cultivars worldwide. In 2006, susceptible infection responses were observed on wheat lines and cultivars carrying Sr24 in a field stem rust screening nursery at Njoro, Kenya. We derived 28 single-pustule isolates from stem rust samples collected from the 2006 Njoro nursery. The isolates were evaluated for virulence on 16 North American stem rust differential lines; on wheat lines carrying Sr24, Sr31, Sr38, and SrMcN; and on a wheat cultivar with a combination of Sr24 and Sr31. All isolates were identified as race TTKS with additional virulence on Sr31 and Sr38. These isolates were divided into two groups: group A (seven isolates and the two control isolates), producing a low infection type, and group B (21 isolates), producing a high infection type on Sr24, respectively. Isolates of group B represented a new variant of race TTKS with virulence to Sr24. Eighteen simple sequence repeat (SSR) markers were used to examine the genetic relationship between these two groups of isolates in race TTKS and five North American races (MCCF, QCCQ, RCRS, RTHS, and TPMK) that are representative of distinct lineage groups. All isolates of race TTKS shared an identical SSR genotype and were clearly different from North American races. The virulence and SSR data indicated that the new variant of race TTKS with Sr24 virulence likely has arisen via mutation within the TTKS genetic lineage. We propose to revise the North American stem rust nomenclature system by the addition of four genes (Sr24, Sr31, Sr38, and SrMcN) as the fifth set. This revision recognizes the virulence on Sr31 and differentiates isolates within race TTKS into two separate races: TTKSK and TTKST, with avirulence and virulence on Sr24, respectively. The occurrence of race TTKST with combined virulence on Sr24 and Sr31 has substantially increased the vulnerability of wheat to stem rust worldwide.

Effects of the Srl5 allele for resistance on development of the stem rust fungus and cellular responses in wheat

1986 ◽  
Vol 64 (3) ◽  
pp. 626-631 ◽  
Author(s):  
H. D. M. Gousseau ◽  
B. J. Deverall
Keyword(s):  
Stem Rust ◽  
Rust Fungus ◽  
Cell Formation ◽  
Cellular Responses ◽  
Host Cells ◽  
Puccinia Graminis ◽  
Wheat Line ◽  
Cell Necrosis ◽  
Virulent Strains ◽  
Mother Cells

The development of avirulent and virulent strains of stem rust (Puccinia graminis Pers. f.sp. tritici Eriks. & Henn.) in a susceptible wheat line and two cultivars bearing the Sr15 allele for resistance was studied, mainly by fluorescence microscopy. Formation of appressoria, substomatal vesicles, infection hyphae, and the first haustorium was unaffected by resistance. The first effect of Sr15 expression was a slower rate of haustorial mother cell formation and was first seen 48 h after inoculation. Effects on hyphal branching and colony radii followed. Necrosis of host cells was first seen at 42 h, but inspection of individual infection sites showed that necrosis did not coincide with effects on haustorial mother cells. It is possible that deterioration of host cells leading to visible host cell necrosis may be related to effects on rust development. Sr15 expression gave a mesothetic reaction, first seen microscopically 60 h after inoculation. Differences between individual infection sites in this reaction may be related to the timing of the onset of necrosis.

CELLULAR CHANGES IN RELATION TO RUST RESISTANCE

1943 ◽  
Vol 21c (5) ◽  
pp. 151-172 ◽  
Author(s):  
F. S. Thatcher
Keyword(s):  
Host Cell ◽  
Regional Differences ◽  
Host Cells ◽  
Puccinia Graminis ◽  
Solute Permeability ◽  
Permeability Changes ◽  
Brown Discoloration ◽  
Plant Stage ◽  
Permeability Increase ◽  
Relationship Of

Concomitant studies of the histopathological development and permeability changes associated with the browning reaction of Kubanka wheat to Puccinia graminis Tritici race 34 shows that the browning symptom is caused by encystment of haustoria and brown discoloration of host cell walls. This reaction is accompanied by a progressive permeability increase of host cells to a degree that probably becomes fatal.Extremes of resistance and of susceptibility manifest in the mesothetic reaction are found to be associated, respectively, with local decrease and increase of solute permeability of the host cell membrane.Cold hardening of wheat plants under some conditions caused a more vigorous development of rust and a slight lessening of resistance symptoms, actions that may be associated with a permeability increase induced by hardening. Hardening to cold did not appreciably alter the relative osmotic relationship of fungus and host.Infection of oats, barley, wheat, and corn with appropriate smuts did not change the degree of susceptibility to specific rusts.Evidence is presented that suggests that resistance of Hope wheat in the mature plant stage may be partly determined by lack of availability of water to the parasites. This may also explain regional differences in susceptibility. These are tentative conclusions only.Vital histological examination of the development of resistant flecks on Vernal wheat demonstrates that host cells are killed prior to the occurrence of any discernible injury to fungus organs.A suggestion is made relative to the cause of the different degrees of permeability change associated with different rust reactions.

scholarly journals Metabolic Signatures of Cryptosporidium parvum-Infected HCT-8 Cells and Impact of Selected Metabolic Inhibitors on C. parvum Infection under Physioxia and Hyperoxia

Biology ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 60
Author(s):  
Juan Vélez ◽  
Zahady Velasquez ◽  
Liliana M. R. Silva ◽  
Ulrich Gärtner ◽  
Klaus Failing ◽  
...  
Keyword(s):  
Host Cell ◽  
Cryptosporidium Parvum ◽  
Cell Metabolism ◽  
Lactate Production ◽  
Glucose Consumption ◽  
Host Cells ◽  
Metabolic Inhibitors ◽  
Low Oxygen ◽  
Metabolic Signatures

Cryptosporidium parvum is an apicomplexan zoonotic parasite recognized as the second leading-cause of diarrhoea-induced mortality in children. In contrast to other apicomplexans, C.parvum has minimalistic metabolic capacities which are almost exclusively based on glycolysis. Consequently, C. parvum is highly dependent on its host cell metabolism. In vivo (within the intestine) infected epithelial host cells are typically exposed to low oxygen pressure (1–11% O2, termed physioxia). Here, we comparatively analyzed the metabolic signatures of C. parvum-infected HCT-8 cells cultured under both, hyperoxia (21% O2), representing the standard oxygen condition used in most experimental settings, and physioxia (5% O2), to be closer to the in vivo situation. The most pronounced effect of C. parvum infection on host cell metabolism was, on one side, an increase in glucose and glutamine uptake, and on the other side, an increase in lactate release. When cultured in a glutamine-deficient medium, C. parvum infection led to a massive increase in glucose consumption and lactate production. Together, these results point to the important role of both glycolysis and glutaminolysis during C. parvum intracellular replication. Referring to obtained metabolic signatures, we targeted glycolysis as well as glutaminolysis in C. parvum-infected host cells by using the inhibitors lonidamine [inhibitor of hexokinase, mitochondrial carrier protein (MCP) and monocarboxylate transporters (MCT) 1, 2, 4], galloflavin (lactate dehydrogenase inhibitor), syrosingopine (MCT1- and MCT4 inhibitor) and compound 968 (glutaminase inhibitor) under hyperoxic and physioxic conditions. In line with metabolic signatures, all inhibitors significantly reduced parasite replication under both oxygen conditions, thereby proving both energy-related metabolic pathways, glycolysis and glutaminolysis, but also lactate export mechanisms via MCTs as pivotal for C. parvum under in vivo physioxic conditions of mammals.

scholarly journals The Campylobacter jejuni CiaD effector co-opts the host cell protein IQGAP1 to promote cell entry

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Nicholas M. Negretti ◽  
Christopher R. Gourley ◽  
Prabhat K. Talukdar ◽  
Geremy Clair ◽  
Courtney M. Klappenbach ◽  
...  
Keyword(s):  
Host Cell ◽  
Campylobacter Jejuni ◽  
Foodborne Pathogen ◽  
Small Gtpase ◽  
Host Cells ◽  
Cell Protein ◽  
Host Cell Protein ◽  
Cell Binding ◽  
Actin Reorganization ◽  
Cell Cytosol

AbstractCampylobacter jejuni is a foodborne pathogen that binds to and invades the epithelial cells lining the human intestinal tract. Maximal invasion of host cells by C. jejuni requires cell binding as well as delivery of the Cia proteins (Campylobacter invasion antigens) to the host cell cytosol via the flagellum. Here, we show that CiaD binds to the host cell protein IQGAP1 (a Ras GTPase-activating-like protein), thus displacing RacGAP1 from the IQGAP1 complex. This, in turn, leads to the unconstrained activity of the small GTPase Rac1, which is known to have roles in actin reorganization and internalization of C. jejuni. Our results represent the identification of a host cell protein targeted by a flagellar secreted effector protein and demonstrate that C. jejuni-stimulated Rac signaling is dependent on IQGAP1.

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