Ultrastructure of compatible and incompatible interactions of soybean roots infected with the plant pathogenic oomycete Phytophthora sojae

1997 ◽  
Vol 75 (9) ◽  
pp. 1493-1508 ◽  
Author(s):  
K. Enkerli ◽  
C. W. Mims ◽  
M. G. Hahn
Keyword(s):  
Host Cell ◽  
Vascular Tissue ◽  
Light And Electron Microscopy ◽  
Phytophthora Sojae ◽  
Host Responses ◽  
Plant Responses ◽  
Cortical Cells ◽  
Wall Appositions ◽  
Race 2 ◽  
Incompatible Interactions

Compatible and incompatible interactions of two soybean isolines containing either Rps1a or Rps1b resistance genes with races 2 and 8 of Phytophthora sojae were examined by light and electron microscopy. Phytophthora sojae race 2 is virulent on Rps1b plants and avirulent on Rps1a plants. Race 8 shows the reverse reaction; it is avirulent on Rps1b plants, but virulent on Rps1a plants. All combinations of races and cultivars were examined at times ranging from 30 min to 20 h postinoculation. Zoospore encystment, germination, and infection occurred within 30 min in all interactions. No evidence of appressorium formation was found. Wall appositions in epidermal cells adjacent to hyphae were very frequent by 30 min postinoculation. Differences between compatible and incompatible interactions became evident as early as 4 h postinoculation. The major difference appeared to relate to timing of host responses, which lead to two different types of relationships. In compatible interactions, P. sojae exhibited a short biotrophic phase with the establishment of many haustoria without triggering visible plant responses in cortical cells until approximately 10 h postinoculation. By 15 h postinoculation, almost the entire root was necrotic, wall appositions were abundant, and vascular tissue was colonized. The incompatible interaction was characterized by a nearly complete absence of haustoria, rapid host cell necrosis, and formation of many wall appositions by 4 h postinoculation. The pathogen rarely penetrated beyond the endodermis of the resistant host and colonization of vascular tissue was rare. Overall there were clear ultrastructural differences between compatible and incompatible interactions of soybean with P. sojae. These data support a strong correlation of resistance with host cell death, formation of wall appositions, and absence of root stele colonization. Key words: Phytophthora sojae, Glycine max, host–pathogen interaction, ultrastructure.

Penetration and colonization of resistant and susceptible Apium graveolens by Fusarium oxysporum f.sp. apii race 2: callose as a structural response

1988 ◽  
Vol 66 (12) ◽  
pp. 2385-2391 ◽  
Author(s):  
C. M. Jordan ◽  
R. M. Endo ◽  
L. S. Jordan
Keyword(s):  
Fusarium Oxysporum ◽  
Host Cell ◽  
Cell Walls ◽  
Vascular Tissue ◽  
Periodic Acid ◽  
Light And Electron Microscopy ◽  
Structural Response ◽  
Aniline Blue ◽  
Apium Graveolens ◽  
Race 2

Root apices of Apium graveolens L. resistant and susceptible to race 2 of Fusarium oxysporum f.sp. apii (R. Nels. & Sherb.) were studied at various times after inoculation, using light and electron microscopy to determine structural response(s) of the hosts during penetration and colonization by the pathogen. Penetration was intercellular and intracellular and involved mechanical and enzymatic mechanisms. At the onset of penetration, the host cell walls manifested fluorescence, induced with either aniline blue or sirofluor, at the point of penetration. The fluorescent area was more intense and larger in the resistant host. Fluorescence disappeared with time. After incubation with β-1,3 glucanase fluorescence disappeared, indicating β-1,3 polysaccharide (probably callose) presence. Callose deposits were 2 and 3 times greater in the epidermis and 4 and 9 times greater in the cortex of the resistant than in two susceptible hosts, respectively. Hyphal counts in the cortex of the resistant host were 50% fewer than in the susceptible hosts. Increased callose deposition on host cell walls was associated with reduced colonization. Callose formed in vascular tissue as the fungus colonized it. Callose detection with sirofluor was more sensitive; background fluorescence common with aniline blue without periodic acid – Schiff's reagent pretreatment was absent.

Resistant responses in juvenile seedlings of Pinus densiflora (Japanese red pine) inoculated with Endocronartium harknessii

1989 ◽  
Vol 67 (12) ◽  
pp. 3545-3552 ◽  
Author(s):  
A. A. Hopkin ◽  
P. V. Blenis ◽  
Y. Hiratsuka
Keyword(s):  
Host Cell ◽  
Vascular Tissue ◽  
Pinus Densiflora ◽  
Light And Electron Microscopy ◽  
Host Cells ◽  
Cortical Cells ◽  
Host Cell Death ◽  
Endocronartium Harknessii ◽  
Infected Cells ◽  
Endodermal Cells

Hypocotyls of Pinus densiflora, a species known to be resistant to western gall rust, were inoculated with Endocronartium harknessii and examined by light and electron microscopy. Host cells, when initially infected, were apparently unaffected, as were the haustoria within them. Seedlings were observed to respond to infection in two ways. In the first type of response, infected cells showed signs of necrosis by 9 days after inoculation, although infecting haustoria appeared normal. By 18 days, most cortical cells in the centre of the infected region were necrotic, as were the haustoria within them. Infected cells at the colony margin still appeared healthy, indicating that host cell necrosis lagged behind infection and only occurred after the haustorium was established. Four weeks after inoculation, a ring of suberized and lignified endodermal cells separated the infected cortex from the uninfected vascular tissue and appeared to prevent further inward growth of the fungus. The second response type involved production of encapsulations around haustoria. Encapsulations appeared to have formed after haustoria senescence and were eventually followed by host cell death.

Infection by Phytophthora cinnamomi Rands of Roots of Eucalyptus calophylla R.Br. and Eucalyptus marginata Donn. ex Sm

1977 ◽  
Vol 25 (5) ◽  
pp. 483 ◽  
Author(s):  
N Malajczuk ◽  
AJ Mccomb ◽  
CA Parker
Keyword(s):  
Phytophthora Cinnamomi ◽  
Light And Electron Microscopy ◽  
Inhibitory Effect ◽  
Lateritic Soil ◽  
Root Damage ◽  
Mature Trees ◽  
Cortical Cells ◽  
Eucalyptus Marginata ◽  
Seedling Roots ◽  
Loam Soil

On lateritic podzolic soils in Western Australia Eucalyptus calophylla is resistant to Phytophthora cinnamomi whereas Eucalyptus marginata is susceptible and eventually killed by the pathogen. On loam soils both eucalypts are resistant. Possible mechanisms for resistance of E. calophylla in lateritic soil and the inhibitory action of loam soils were investigated. Aseptically raised eucalypt seedlings succumbed to infection in liquid culture tubes. The mechanism of infection was compared by light and electron microscopy which showed similar fungal invasion and penetration into roots of both eucalypt species. Vegetative hyphae initially penetrated intercellularly and proliferated rapidly within cortical and stelar tissue. Intracellular invasion of these tissues occurred 48hr after initial infection through dissolution of the host cell wall. Chlamydospores were formed within a number of cortical cells. Unsuberized roots of mature trees produced aseptically showed reactions to invasion similar to those of the eucalypt seedling roots. Suberized roots were not invaded. The addition of small quantities of lateritic soil to sterile sand so as to introduce soil micro-organisms without altering the chemical and physical status of the sand, and subsequent inoculation of the sand with P.cinnamomi, resulted in a reduction of root damage on both eucalypts when compared with seedlings raised in sterile sand. Roots of E.calophylla were less severely damaged than those of E.marginata. The addition of small quantities of loam soil significantly reduced root damage in seedlings of both species. These results parallel both pot experiments and field observations, and suggest that microorganisms of the rhizosphere may be an important factor in the resistance of E.calophylla to infection, and in the inhibitory effect of loam soil on P.cinnamomi.

scholarly journals Adaptation to host cell environment during experimental evolution of Zika virus

2020 ◽  
Author(s):  
Vincent Grass ◽  
Emilie Hardy ◽  
Kassian Kobert ◽  
Soheil Rastgou Talemi ◽  
Elodie Décembre ◽  
...  
Keyword(s):  
Host Cell ◽  
Human Health ◽  
Zika Virus ◽  
Viral Evolution ◽  
Time Lag ◽  
Viral Escape ◽  
Host Responses ◽  
Type I ◽  
Zikv Infection ◽  
Antiviral Responses

AbstractZika virus (ZIKV) infection can cause developmental and neurological defects and represents a threat for human health. Type I/III interferon responses control ZIKV infection and pathological processes, yet the virus has evolved various mechanisms to defeat these host responses. Here, we established a pipeline to delineate at high-resolution the genetic evolution of ZIKV in a controlled host cell environment. We uncovered that serially passaged ZIKV acquired increased infectivity, defined as the probability for one virus to initiate infection, and simultaneously developed a resistance to TLR3-induced restriction. We built a mathematical model that suggests that the increased infectivity is due to a reduced time-lag between infection and viral replication. We found that this adaptation is cell-type specific, suggesting that different cell environments may drive viral evolution along different routes. Deep-sequencing of ZIKV quasi-species pinpointed mutations whose increased frequencies temporally coincide with the acquisition of the adapted phenotype. We functionally validated a point-mutation in ZIKV envelope (E) protein recapitulating the adapted phenotype. Its positioning on the E structure suggests a putative function in protein refolding/stability. Altogether, our results uncovered ZIKV adaptations to the cell environment leading to an accelerated replication onset coupled with resistance to TLR3-induced antiviral response. Our work provides insights into viral escape mechanisms and interactions with host cell and can serve as a framework to study other viruses.Significance StatementZika virus poses a major threat to Human health worldwide. To understand how Zika virus interacts with human cells, we studied its evolution in cell cultures. We found that the viruses adapted by initiating their replication sooner after cell entry. We sequenced the genomes of the viruses evolved over time and found mutations underlying the adaptation of the virus. One mutation in the envelope viral protein is sufficient to reproduce the faster initiation of replication. Our multidisciplinary approach based on analyzing viral evolution in a controlled environment and mathematical modeling revealed how Zika virus can escape antiviral responses, and can serve as framework to study other viruses.

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.

scholarly journals Histological Comparison of Fibrous Root Infection of Disease-Tolerant and Susceptible Citrus Hosts by Phytophthora nicotianae and P. palmivora

1998 ◽  
Vol 88 (5) ◽  
pp. 389-395 ◽  
Author(s):  
T. L. Widmer ◽  
J. H. Graham ◽  
D. J. Mitchell
Keyword(s):  
Light And Electron Microscopy ◽  
Cellular Responses ◽  
Poncirus Trifoliata ◽  
Phytophthora Nicotianae ◽  
Sour Orange ◽  
Trifoliate Orange ◽  
Fibrous Root ◽  
Cortical Cells ◽  
Phytophthora Spp ◽  
Fibrous Roots

Phytophthora nicotianae and P. palmivora infect and cause rot of fibrous roots of susceptible and tolerant citrus rootstocks in Florida orchards. The infection and colonization by the two Phytophthora spp. of a susceptible citrus host, sour orange (Citrus aurantium), and a tolerant host, trifoliate orange (Poncirus trifoliata), were compared using light and electron microscopy. Penetration by both Phytophthora spp. occurred within 1 h after inoculation, regardless of the host species. No differences were observed in mode of penetration of the hypodermis or the hosts' response to infection. After 24 h, P. palmivora had a significantly higher colonization of cortical cells in susceptible sour orange than in tolerant trifoliate orange. Intracellular hyphae of both Phytophthora spp. were observed in the cortex of sour orange, and cortical cells adjacent to intercellular hyphae of P. palmivora were disrupted. In contrast, the cortical cells of sour orange and trifoliate orange adjacent to P. nicotianae hyphae and the cortical cells of trifoliate orange adjacent to P. palmivora were still intact. After 48 h, the cortical cells of both hosts adjacent to either Phytophthora spp. were disrupted. After 48 and 72 h, P. palmivora hyphae colonized the cortex of sour orange more extensively than the cortex of trifoliate orange; P. palmivora also colonized both hosts more extensively than P. nicotianae. A higher rate of electrolyte leakage among host-pathogen combinations reflected the combined effects of greater cell disruption by P. palmivora than by P. nicotianae, and the higher concentration of electrolytes in healthy roots of trifoliate orange than of sour orange. Although cellular responses unique to the tolerant host were not observed, reduced hyphal colonization by both pathogens in the cortex of trifoliate orange compared with sour orange is evidence for a putative resistance factor(s) in the trifoliate orange roots that inhibits the growth of Phytophthora spp.

scholarly journals The Avr1b Locus of Phytophthora sojae Encodes an Elicitor and a Regulator Required for Avirulence on Soybean Plants Carrying Resistance Gene Rps1b

2004 ◽  
Vol 17 (4) ◽  
pp. 394-403 ◽  
Author(s):  
Weixing Shan ◽  
Minh Cao ◽  
Dan Leung ◽  
Brett M. Tyler
Keyword(s):  
Resistance Gene ◽  
Artificial Chromosome ◽  
Phytophthora Sojae ◽  
Secreted Protein ◽  
Bac Clone ◽  
Bac Contig ◽  
Soybean Plants ◽  
Substitution Mutations ◽  
Race 2 ◽  
Soybean Leaves

We have used map-based approaches to clone a locus containing two genes, Avr1b-1 and Avr1b-2, required for avirulence of the oomycete pathogen Phytophthora sojae (Kaufmann & Gerdemann) on soybean plants carrying resistance gene Rps1b. Avr1b-1 was localized to a single 60-kb bacterial artificial chromosome (BAC) clone by fine-structure genetic mapping. Avr1b-1 was localized within the 60-kb region by identification of an mRNA that is expressed in a race-specific and infection-specific manner and that encodes a small secreted protein. When the Avr1b-1 protein was synthesized in the yeast Pichia pastoris and the secreted protein infiltrated into soybean leaves, it triggered a hypersensitive response specifically in host plants carrying the Rps1b resistance gene. This response eventually spread to the entire inoculated plant. In some isolates of P. sojae virulent on Rps1b-containing cultivars, such as P7081 (race 25) and P7076 (race 19), the Avr1b-1 gene had numerous substitution mutations indicative of strong divergent selection. In other isolates, such as P6497 (race 2) and P9073 (race 25), there were no substitutions in Avr1b-1, but Avr1b-1 mRNA did not accumulate. Genetic complementation experiments with P6497 revealed the presence of a second gene, Avr1b-2, required for the accumulation of Avr1b-1 mRNA. Avr1b-2 was genetically mapped to the same BAC contig as Avr1b-1, using a cross between P7064 (race 7) and P6497. The Avr1k gene, required for avirulence on soybean cultivars containing Rps1k, was mapped to the same interval as Avr1b-1.

scholarly journals Effect of Temperature on and Histopathology of the Interaction Between Meloidogyne incognita and Thielaviopsis basicola on Cotton

1999 ◽  
Vol 89 (8) ◽  
pp. 613-617 ◽  
Author(s):  
N. R. Walker ◽  
T. L. Kirkpatrick ◽  
C. S. Rothrock
Keyword(s):  
Meloidogyne Incognita ◽  
Vascular Tissue ◽  
Root Surface ◽  
Effect Of Temperature ◽  
Infested Soil ◽  
Thielaviopsis Basicola ◽  
Root Knot Nematode ◽  
Cortical Cells ◽  
Node Ratio ◽  
Cotton Seeds

Controlled environments were used to study the relationship between the root-knot nematode (Meloidogyne incognita) and Thielaviopsis basicola on cotton. Temperature treatments were continuous 20, 24, and 28°C or two cyclic linear regimes with ranges of 14 to 32 or 18 to 28°C over 24 h. Cotton seeds were planted in fumigated soil infested with T. basicola, M. incognita, or both. After 42 days, pathogen effects on plant growth and pathogen development were evaluated. Histology was conducted on roots collected 14, 28, and 42 days after planting in the continuous 24°C treatment. Reductions in plant height-to-node ratio and total fresh weight were observed for soils infested with both pathogens compared with the control or with soils infested with either pathogen, except for M. incognita-infested soil at 28°C. T. basicola reduced root galling and reproduction of the nematode at all temperatures. Vascular discoloration caused by T. basicola was greater in the presence of M. incognita compared with that by T. basicola alone. At 2 and 4 weeks, histological studies showed that plants grown in all T. basicola-infested soils contained chlamydospore chains on the root surface and in cortical cells. The fungus was not observed inside the vascular cylinder. Roots from 4-week-old plants from soils infested with T. basicola and M. incognita showed fungal sporulation in vascular tissue and localized necrosis of vascular tissue adjacent to the nematodes. At 6 weeks, plants grown in soil infested with T. basicola alone exhibited no remaining cortical tissue and no evidence of vascular colonization by the fungus. Six-week-old plants grown in T. basicola + M. incognita-infested soils exhibited extensive vascular necrosis and sporulation within vascular tissue. These studies suggest that coinfection expands the temperature ranges at which the pathogens are able to cause plant damage. Further, M. incognita greatly increases the access of T. basicola to vascular tissue.

Structural Characterization of the Cell Division Cycle in Strigomonas culicis, an Endosymbiont-Bearing Trypanosomatid

2014 ◽  
Vol 20 (1) ◽  
pp. 228-237 ◽  
Author(s):  
Felipe Lopes Brum ◽  
Carolina Moura Costa Catta-Preta ◽  
Wanderley de Souza ◽  
Sergio Schenkman ◽  
Maria Carolina Elias ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Host Cell ◽  
Light And Electron Microscopy ◽  
Three Dimensional ◽  
Symbiotic Bacterium ◽  
Single Copy ◽  
Cell Structures ◽  
Dimensional Reconstruction ◽  
Protozoan Cell

AbstractStrigomonas culicis (previously referred to as Blastocrithidia culicis) is a monoxenic trypanosomatid harboring a symbiotic bacterium, which maintains an obligatory relationship with the host protozoan. Investigations of the cell cycle in symbiont harboring trypanosomatids suggest that the bacterium divides in coordination with other host cell structures, particularly the nucleus. In this study we used light and electron microscopy followed by three-dimensional reconstruction to characterize the symbiont division during the cell cycle of S. culicis. We observed that during this process, the symbiotic bacterium presents different forms and is found at different positions in relationship to the host cell structures. At the G1/S phase of the protozoan cell cycle, the endosymbiont exhibits a constricted form that appears to elongate, resulting in the bacterium division, which occurs before kinetoplast and nucleus segregation. During cytokinesis, the symbionts are positioned close to each nucleus to ensure that each daughter cell will inherit a single copy of the bacterium. These observations indicated that the association of the bacterium with the protozoan nucleus coordinates the cell cycle in both organisms.

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.

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