Ultrastructure of Cells in Toxin-Treated and Helminthosporium sacchari-Infected Sugarcane Leaves

Strobel, Gary A.; Hess, W. M.; Steiner, G.

doi:10.1094/phyto-62-339

Cited by 23 publications

(4 citation statements)

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“…9 the chloroplasts and particularly the nucleus seem more resistant to disintegration, although both these organelles are deteriorating. Similar-appearing chloroplasts have been observed in other host-parasite combinations (9,14,16). The difficulty in identifying membranes such as the plasma membrane and tonoplast in Fig.…”

Section: Cytoplasmic and N~rclear Cl~angessupporting

confidence: 69%

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The ultrastructure of M1-a-mediated resistance to powdery mildew infection in barley

Edwards¹

1975

Can. J. Bot.

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EDWARDS, H. H. 1975. The ultrastructure of MI-a-mediated resistance to powdery mildew infection in barley. Can. J. Bot. 53: 2589-2597. MI-a-mediated resistance in barley to invasion by the CR3 race of Etysiplle grarninis f. sp. hordei does not occur in every host cell with the same speed and severity. In some cells ultrastructural changes within the host cell as a result of resistance will occur within 24 h after inoculation, whereas in other cells these changes may take up to 72 h. In some cells the ultrastructural changes are so drastic that they give the appearance of a hypersensitive death of the host cell, whereas in other cells the changes are very slight. In any case, at the end of these changes the fungus ceases growth. The ultrastructural changes occur in penetrated host epidermal cells as well as non-infected adjacent epidermal and mesophyll cells.The following ultrastructural changes have been observed: (I) an electron-dense material which occurs either free in the vacuole or adhering to the tonoplast (the material is granular or in large clumps); (2) an increased electron density of the host cytoplasm and nucleus; (3) a breakdown of the tonoplast so that the cytoplasmic constituents become dispersed throughout the cell lumen; and (4) the deposition of papillar-like material in areas other than the penetration site. The first three changes take place within the host cell protoplasts andare directly attributable to the gene MI-a. These changes are typical of stressor incompatibility responses and thus MI-a appears to trigger a generalized incompatibility response in the presence of race CR3. The papillar-like material occurs outside the host cell protoplast in the same manner as the papilla and probably is not directly attributable to MI-a. EDWARDS, H. H. 1975. The ultrastructure of MI-[I-mediated resistance to powdery mildew infection in barley. Can. J. Bot. 53: 2589-2597. Chez I'orge, la resistance d'origine MI-a a I'invasion par la race CR3 d'Erysiphe grar~ritlis f. sp. 11ordei.ne s'effectue pas dans toutes les cellules avec la mtme vitesse et avec la mtme intensite. Chez certaines cellules, les changements ultrastructuraux dans la cellule-hbte, resultant de la resistance, ont lieu moins de 24 h apres I'inoculation, alors que dans les autres cellules ces changements peuvent prendre jusqu'i 72 h. Dans certaines cellules les changements ultrastructuraux sont tellement brutaux qu'ils prennent I'apparence d'une mortalit6 par hypersensibilite de la cellule-hbte, alors que dans d'autres cellules les changements sont minimes. Dans tous les cas, la croissance du champignon s'arrtte avec la fin de ces changements. Les changements ultrastructuraux se manifestent dans les cellules epidermiques que penetre le champignon, aussi'bien que dans les cellules adjacentes non infectkes de I'epiderme et du mksophylle.L'auteur a observe les changements ultrastructuraux suivants: (1) un materiel dense aux electtons qui se forme libre dans la vacuole ou accole au tonoplaste; ce materiel est granulaire ou sous forme de gros...

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Section: Cytoplasmic and N~rclear Cl~angessupporting

confidence: 69%

“…One possibility which others have previously suggested (12,14) is the activation of host cell lysosomes. If this is the case, then resistance mediated by the M1-a gene is accomplished by activating the host cell's normal senescence or stress response.…”

Section: Cj7anges In Non-infected Host Cellsmentioning

confidence: 99%

The ultrastructure of M1-a-mediated resistance to powdery mildew infection in barley

Edwards¹

1975

Can. J. Bot.

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“…Strobel et al (4,5) postulated that the toxin affected cellular membranes accounting for the initial water-soaking symptoms expressed in toxin-treated tissues. One of the first ultrastructural changes observed in treated tissues was alterations in chloroplast membranes.…”

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confidence: 99%

Biochemical Basis of the Resistance of Sugarcane to Eyespot Disease

Strobel

1973

Proc. Natl. Acad. Sci. U.S.A.

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Helminthosporoside is the host-specific toxin produced by Helminthosporium sacchari , the organism causing eyespot disease on sugarcane. Clones of sugarcane susceptible to the toxin posses a membrane protein that binds the toxin. Membranes of resistant clones do not bind the toxin. In this study, a binding protein from a susceptible clone was compared with its counterpart from a resistant clone. The protein from the resistant clone did not bind the toxin unless it was first treated with mild detergent. The two proteins are antigenically identical, have the same molecular weight, and each contains four subunits. They differ slightly in their electrophoretic mobility and vary with respect to four different aminoacid residues. The basis of resistance of clone H50-7209 to eyespot disease is directly associated with the structurally altered membrane-binding protein.

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“…Swelling of the outer chloroplast membranes, intergranal membranes and granal stacks, as well as total breaks in the outer membranes with release of the contents into the cytoplasm have been observed in plants exposed to other fungus toxins, bacterial metabolites or other conditions that cause chlorosis, including such toxins as tentoxin [18], tabtoxin [19], tagetitoxin [17], helminthosporoside [20], or the build-up of ammonia levels in tissues [21]. Vesiculation of thylakoids has been reported as an effect of tentoxin on morning glory [22].…”

Section: Discussionmentioning

confidence: 99%

Effects ofFusarium solani naphthazarin toxins on the cytology and ultrastructure of rough lemon seedlings

1993

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Abstract. Two naphthazarin phytotoxins (dihydrofusarubin and isomarticin) produced by Fusariurn solani were used to determine their effects on the cytology of leaves of rough lemon (Citrus jambhiri Lush) seedlings maintained in a dilute solution of the toxins. Dihydrofusarubin alone or in combination with isomarticin (80:20, v/v) caused cell necrosis above the midveins and lateral veins, plasmolysis or collapse of spongy mesophyll cells, collapse of phloem, depletion of starch, swelling of chloroplasts and disruption of cellular organization. At the ultrastructural level, the toxins affected chloroplast membranes by causing swelling, breaks in outer membranes, granal stack disorganization and swelling of intergranal membranes. The interstromal lamellae appeared as vesicles and sometimes as peripheral reticulum, with an increase in plastoglobuli. The tonoplast was broken or vesiculated. The only membranes not affected by the toxins were those of the nucleus and the mitochondria. This study establishes that the initial toxin effects of these fungal phytotoxins are on organellar membranes, primarily those of the chloroplasts, plasmalemma and tonoplast.

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Ultrastructure of Cells in Toxin-Treated and Helminthosporium sacchari-Infected Sugarcane Leaves

Cited by 23 publications

References 0 publications

The ultrastructure of M1-a-mediated resistance to powdery mildew infection in barley

The ultrastructure of M1-a-mediated resistance to powdery mildew infection in barley

Biochemical Basis of the Resistance of Sugarcane to Eyespot Disease

Effects ofFusarium solani naphthazarin toxins on the cytology and ultrastructure of rough lemon seedlings

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