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.

THE PHYSIOLOGY OF HOST–PARASITE RELATIONS: XVIII. DISTRIBUTION OF TRITIUM-LABELLED CYTIDINE, URIDINE, AND LEUCINE IN WHEAT LEAVES INFECTED WITH THE STEM RUST FUNGUS

1967 ◽  
Vol 45 (5) ◽  
pp. 555-563 ◽  
Author(s):  
P. K. Bhattacharya ◽  
Michael Shaw
Keyword(s):  
Stem Rust ◽  
Rust Fungus ◽  
Host Cells ◽  
Fungal Mycelium ◽  
Puccinia Graminis ◽  
Mesophyll Cells ◽  
Wheat Leaves ◽  
Host Parasite

Wheat leaves were detached 6 days after inoculation with the stem rust fungus (Puccinia graminis var. tritici Erikss. and Henn.) and fed with tritiated leucine, cytidine, uridine, or thymidine. Mesophyll cells in infected zones incorporated more leucine into protein and more cytidine and uridine into RNA than did cells in adjacent uninfected tissue. Leucine, cytidine, and uridine were also heavily incorporated by fungal mycelium and developing uredospores. Grain counts over host nuclei in the infected zone were two to three-fold of those over nuclei in adjacent uninfected zones. There was no detectable incorporation of thymidinemethyl-3H into either the fungus or the host cells. The results are discussed.

scholarly journals Different Cell Wall-Degradation Ability Leads to Tissue-Specificity between Xanthomonas oryzae pv. oryzae and Xanthomonas oryzae pv. oryzicola

Pathogens ◽  
2020 ◽  
Vol 9 (3) ◽  
pp. 187
Author(s):  
Jianbo Cao ◽  
Chuanliang Chu ◽  
Meng Zhang ◽  
Limin He ◽  
Lihong Qin ◽  
...  
Keyword(s):  
Cell Wall ◽  
Tissue Specificity ◽  
Mesophyll Cell ◽  
Xanthomonas Oryzae ◽  
Cell Wall Degradation ◽  
Intercellular Spaces ◽  
Mesophyll Cells ◽  
Degradation Ability

Xanthomonas oryzae pv. oryzae (Xoo) and Xanthomonas oryzae pv. oryzicola (Xoc) lead to the devastating rice bacterial diseases and have a very close genetic relationship. There are tissue-specificity differences between Xoo and Xoc, i.e., Xoo only proliferating in xylem vessels and Xoc spreading in intercellular space of mesophyll cell. But there is little known about the determinants of tissue-specificity between Xoo and Xoc. Here we show that Xoc can spread in the intercellular spaces of mesophyll cells to form streak lesions. But Xoo is restricted to growth in the intercellular spaces of mesophyll cells on the inoculation sites. In vivo, Xoc largely breaks the surface and inner structures of cell wall in mesophyll cells in comparison with Xoo. In vitro, Xoc strongly damages the cellulose filter paper in comparison with Xoo. These results suggest that the stronger cell wall-degradation ability of Xoc than that of Xoo may be directly determining the tissue-specificity.

Tropospheric ozone-induced structural changes in leaf mesophyll cell walls in grapevine plants

Biologia ◽  
2006 ◽  
Vol 61 (1) ◽  
Author(s):  
Nikola Ljubešić ◽  
Mihaela Britvec
Keyword(s):  
Cell Wall ◽  
Tropospheric Ozone ◽  
Cell Walls ◽  
Structural Changes ◽  
Mesophyll Cell ◽  
Ambient Air ◽  
Vitis Vinifera L ◽  
Mesophyll Cells ◽  
Ozone Concentrations ◽  
Leaf Mesophyll

AbstractThe structural changes in leaves of grapevine plants (Vitis vinifera L.) exposed to different ozone concentrations were investigated. Ozone fumigations were performed in open-top chambers at four different ozone levels (charcoal-filtered air (F), ambient air (N), ambient air + 25 mm3m−3 ozone (O-25) and ambient air + 50 mm3m−3 ozone (O-50)).The leaves of plants from chambers with increased ozone concentrations (O-25 and O-50) were significantly thicker than the controls (F), owing to increased thickness of the mesophyll layer. Observing O-50 leaves, it was found that the mesophyll cell wall displayed structural changes. In some places cell wall thickness increased up to 1 µm. We found callose deposits on the inner side of the cell walls of mesophyll cells. These data are in accord with the concept that the mesophyll cell wall acts as a barrier against the penetration of tropospheric ozone into the cells.

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.

Studies on the haustorium of Castilleja (Scrophulariaceae). II. The endophyte

1973 ◽  
Vol 51 (5) ◽  
pp. 923-931 ◽  
Author(s):  
David R. Dobbins ◽  
Job Kuijt
Keyword(s):  
Cell Wall ◽  
Host Cell ◽  
Light Microscope ◽  
Cell Walls ◽  
Host Cells ◽  
Electron Microscopic ◽  
Cortical Cells ◽  
Host Cell Wall ◽  
Dark Staining ◽  
Host Tissues

The portion of the Castilleja haustorium within the host, the endophyte, was examined at the light-and electron-microscopic levels. The endophyte consists of a stalk of lipid-containing cells and digitate cells at its tip. Vessels run the length of the endophyte. There is a harmonious meshing between host cortical cells and those of the endophyte flank, suggesting that penetration is accomplished, in part, by cell dissolution. Crushing of cells also occurs during endophyte invasion as host phloem tissues are severely buckled and cell walls are greatly folded. Some features of digitate cells include dense cytoplasm, an abundance of endoplasmic reticulum, lateral walls that are thickened as well as those on the side adjacent to the host, and an ability to conform to the contours of host tissues. Often digitate cells are divided by very thin walls that are hardly visible under the light microscope. It is suggested that the thick cell walls may function as "free space" in the absorption of materials from the host. Within the endophyte, vessels differentiate and may contain either a finely granular, dark-staining material or a more coarsely granular, light-staining material. The particles of the latter have irregular shapes. Although granular materials are thus carried by some vessels, cells resembling the structurally intermediate "phloeotracheids" were not seen. Connections through the cell wall were not observed between parasite and host; however, within the endophyte plasmodesmata were highly branched and often contained median nodules. Transfer-like cells which have irregularly thickened walls occurred in the endophyte. Host tissues next to digitate cells appeared to be in a degraded state. Invaginations of the plasmalemma were common and small flattened vesicles were formed in some host cells from the disrupted tonoplast. In several instances, the cytoplasm had receded from the host cell wall and a "beaded" material was present in both vacuoles and large vesicles. The host cell wall at times had a very loose fibrillar appearance. Some host tracheids were occluded with a dense and dark-staining material. The xylem strands of the parasite are connected to the host xylem either by cell wall dissolution or by actual penetration of a digitate cell into a host xylary cell. The penetrating cell subsequently differentiates into a vessel member. A summary and general discussion are given to relate the two portions of the haustorium, the upper haustorium and the endophyte. The mass of new information gained in this study leads us to encourage the application of plastic embedding and sectioning techniques to further light-microscope studies on haustoria.

Ultrastructure and Senescence in an Achloroplastic Mutant of Hordeum vulgare L. cv. Dyan

1992 ◽  
Vol 50 (1) ◽  
pp. 844-845
Author(s):  
R.H.M. Cross ◽  
C.E.J. Botha ◽  
A.K. Cowan ◽  
B.J. Hartley
Keyword(s):  
Cell Wall ◽  
Hordeum Vulgare ◽  
Leaf Tissue ◽  
Ultrastructural Changes ◽  
Hordeum Vulgare L ◽  
Mesophyll Cells ◽  
Lethal Mutant ◽  
Cytoplasmic Matrix ◽  
Close Proximity ◽  
Pinocytotic Vesicles

Senescence is an ordered degenerative process leading to death of individual cells, organs and organisms. The detection of a conditional lethal mutant (achloroplastic) of Hordeum vulgare has enabled us to investigate ultrastructural changes occurring in leaf tissue during foliar senescence.Examination of the tonoplast structure in six and 14 day-old mutant tissue revealed a progressive degeneration and disappearance of the membrane, apparently starting by day six in the vicinity of the mitochondria associated with the degenerating proplastid (Fig. 1.) where neither of the plastid membrane leaflets is evident (arrows, Fig. 1.). At this stage there was evidence that the mitochondrial membranes were undergoing retrogressive changes, coupled with disorganization of cristae (Fig. 2.). Proplastids (P) lack definitive prolamellar bodies. The cytoplasmic matrix is largely agranular, with few endoplasmic reticulum (ER) cisternae or polyribosomal aggregates. Interestingly, large numbers of actively-budding dictysomes, associated with pinocytotic vesicles, were observed in close proximity to the plasmalemma of mesophyll cells (Fig. 3.). By day 14 however, mesophyll cells showed almost complete breakdown of subcellular organelle structure (Fig. 4.), and further evidence for the breakdown of the tonoplast. The final stage of senescence is characterized by the solubilization of the cell wall due to expression and activity of polygalacturonase and/or cellulose. The presence of dictyosomes with associated pinocytotic vesicles formed from the mature face, in close proximity to both the plasmalemma and the cell wall, would appear to support the model proposed by Christopherson for the secretion of cellulase. This pathway of synthesis is typical for secretory glycoproteins.

Haustorial development of Peronospora tabacina infecting Nicotiana tabacum

1983 ◽  
Vol 61 (12) ◽  
pp. 3444-3453 ◽  
Author(s):  
R. N. Trigiano ◽  
C. G. Van Dyke ◽  
H. W. Spurr Jr.
Keyword(s):  
Cell Wall ◽  
Toluidine Blue ◽  
Mesophyll Cell ◽  
Wall Layer ◽  
Peronospora Tabacina ◽  
Host Cytoplasm ◽  
Transmission Electron ◽  
Mold Fungus ◽  
Host Cell Wall ◽  
Hyphal Wall

The development of haustoria in tobacco by the blue-mold fungus Peronospora tabacina was examined using light, scanning, and transmission electron microscopy. Electron-lucent, callose-like appositions were observed between the host plasmalemma and the host mesophyll cell wall prior to haustorial penetration. An electron-opaque penetration matrix was present between the apposition and the host cell wall. The intercellular hyphal wall consisted of two layers which differed in staining quality. The haustorial wall was also two layered, but was primarily composed of and continuous with the inner wall layer of the intercellular hypha. Haustoria were either finger-like or branched and were encased with callose-like material. Most encasements were thickened at the proximal regions of haustoria but were thinner along the distal portions. Vesicles were present in host cytoplasm and were occasionally attached to the invaginated host plasmalemma. These vesicles might contribute to the deposition of the encasement material. The encasement stained positively for callose using aniline blue; calcofluor and toluidine blue O tests for cellulose were inconclusive, and lignin was not detected using toluidine blue O or phloroglucinol–HCl.

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.

scholarly journals Tobacco mosaic virus: a pioneer to cell–to–cell movement

1999 ◽  
Vol 354 (1383) ◽  
pp. 637-643 ◽  
Author(s):  
Vitaly Citovsky
Keyword(s):  
Cell Wall ◽  
Tobacco Mosaic Virus ◽  
Mosaic Virus ◽  
Movement Protein ◽  
Cell Movement ◽  
Host Cells ◽  
Specific Cell ◽  
Viral Movement Protein ◽  
Rna Molecules ◽  
Rna Complexes

Cell–to–cell movement of tobacco mosaic virus (TMV) is used to illustrate macromolecular traffic through plant intercellular connections, the plasmodesmata. This transport process is mediated by a specialized viral movement protein, P30. In the initially infected cell, P30 is produced by transcription of a subgenomic RNA derived from the invading virus. Presumably, P30 then associates with a certain proportion of the viral RNA molecules, sequestering them from replication and mediating their transport into neighbouring uninfected host cells. This nucleoprotein complex is targeted to plasmodesmata, possibly via interaction with the host cell cytoskeleton. Prior to passage through a plasmodesma, the plasmodesmal channel is dilated by the movement protein. It is proposed that targeting of P30–TMV RNA complexes to plasmodesmata involves binding to a specific cell wall–associated receptor molecule. In addition, a cell wall–associated protein kinase, phosphorylates P30 at its carboxy–terminus and minimizes P30–induced interference with plasmodesmatal permeability during viral infection.

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