The interface between the powdery mildew haustorium and the cytoplasm of the susceptible barley epidermal cell

1974 ◽  
Vol 20 (11) ◽  
pp. 1475-1478 ◽  
Author(s):  
W. E. McKeen
Keyword(s):  
Powdery Mildew ◽  
Thin Layer ◽  
Epidermal Cell ◽  
Erysiphe Graminis ◽  
Host Cytoplasm ◽  
Host Parasite

The host–parasite interface separating the haustorium of Erysiphe graminis and the cytoplasm of the barley epidermal cell is an invaginated portion of the host plasmalemma which becomes thicker, more osmophilic, highly invaginated toward the haustorium, and which loses its transparent central stratum. This extrahaustorial membrane is always 1–4 μm distant from the haustorial wall and at first is covered with a thin layer of normal cytoplasm. Later, the host cytoplasm greatly increases in volume, becomes much less dense, and organelles become less confined.

Gene-for-gene interactions between the rye mildew fungus and wheat cultivars

Genome ◽  
1994 ◽  
Vol 37 (5) ◽  
pp. 758-762 ◽  
Author(s):  
Y. Tosa
Keyword(s):  
Triticum Aestivum ◽  
Powdery Mildew ◽  
Chinese Spring ◽  
Single Gene ◽  
Erysiphe Graminis ◽  
Gene Interactions ◽  
Wheat Cultivars ◽  
Genetic Mechanisms ◽  
Host Parasite ◽  
Gene For Gene

Genetic mechanisms of the incompatibility between Erysiphe graminis f.sp. secalis and wheat cultivars were analyzed using F1 hybrids between E. graminis f.sp. secalis, Sk-1, and f.sp. tritici, Tk-1. The avirulence of Sk-1 on Triticum aestivum 'Norin 4', 'Chinese Spring', and 'Kokeshi-komugi' was controlled by a single gene. The resistance of the three cultivars to Sk-1 was also controlled by a single gene, Pm15, a gene for resistance to E. graminis f.sp. agropyri. Implications of these results were discussed in terms of host–parasite coevolution.Key words: powdery mildew, Erysiphe graminis, resistance, wheat.

Relations between haustoria of Erysiphe graminis and host cytoplasm in cells opened by microsurgery

1974 ◽  
Vol 52 (5) ◽  
pp. 987-998 ◽  
Author(s):  
Timothy P. Sullivan ◽  
W. R. Bushnell ◽  
J. B. Rowell
Keyword(s):  
Hordeum Vulgare ◽  
Thin Layer ◽  
Host Cell ◽  
Fungal Growth ◽  
Functional Condition ◽  
Erysiphe Graminis ◽  
Hordeum Vulgare L ◽  
Host Cytoplasm ◽  
Visible Condition ◽  
The Times

Epidermal cells of barley (Hordeum vulgare L.), which contained haustoria of Erysiphe graminis [DC] Merat f. sp. hordei Em. Marchal, were opened with a microneedle, thereby exposing the haustorial apparatus and surviving components of the host protoplast to externally supplied osmotica. Haustoria remained alive and functional for one or more hours in the incised cell with either salt or sucrose osmotica, as indicated by growth of attached hyphae and the visible condition of the haustorium. A thin layer of host cytoplasm (the haustorial sac) remained in place around the functional haustoria. Additional host cytoplasm was seen frequently in streams, masses, or a parietal layer within 100 μm of the haustorium. The cytoplasm often migrated to the haustorium after incision and came to rest there, especially on osmotica hypertonic to the host. The amount of fungal growth after incision was positively correlated with the amount of cytoplasm near the haustorium (large amounts if cells were incised 30 μm or more from the haustorium; small amounts if cells were incised less than 10 μm from the haustorium). The times after incision that cytoplasmic organelles near the haustorium moved in streams or vibratory patterns coincided with the times after incision that hyphae grew. Most of the host cytoplasm was removed from the vicinity of the haustorium when the microneedle was swept past the haustorium repeatedly. However, the haustoria that survived in a functional condition after nearby regions of the host cell had been swept, remained enclosed by a thin layer of cytoplasm and in contact with a layer of host cytoplasm on the host wall around the haustorial neck. The results suggest that the haustorium must be in contact with small amounts of living host cytoplasm to be functional, but that the haustorium does not depend on vacuolar substances, the nucleus of the host, or cytoplasm in distant parts of the host cell.

Cloning and Characterization of a Novel Wheat Glycoside Hydrolase Gene TaGlc2 Induced by Powdery Mildew Pathogen (Erysiphe graminis) Infection

2009 ◽  
Vol 35 (5) ◽  
pp. 786-794
Author(s):  
N PUDAKE Ramesh ◽  
Ming-Ming XIN ◽  
Yu-Jing YIN ◽  
Chao-Jie XIE ◽  
Zhong-Fu NI ◽  
...  
Keyword(s):  
Powdery Mildew ◽  
Glycoside Hydrolase ◽  
Erysiphe Graminis ◽  
Powdery Mildew Pathogen

Changes in sterol composition with ontogeny of Blumeria graminis conidia

2000 ◽  
Vol 78 (10) ◽  
pp. 1288-1293 ◽  
Author(s):  
Jérôme Muchembled ◽  
Anissa Lounès-Hadj Sahraoui ◽  
Anne Grandmougin-Ferjani ◽  
Michel Sancholle
Keyword(s):  
Powdery Mildew ◽  
Plant Pathogen ◽  
Total Sterol ◽  
Sterol Composition ◽  
Blumeria Graminis ◽  
Erysiphe Graminis ◽  
Qualitative And Quantitative ◽  
Wheat Powdery Mildew

The total sterol composition of conidia of the obligate plant pathogen Blumeria (= Erysiphe) graminis f.sp. tritici has been analysed as a function of their ontogeny during sporulation. Two main classes of sterols were characterized: 24-ethylsterols (24-ethylcholesta-5,22-dienol, 24-ethylcholesterol, and Δ5-avenasterol) and 24-methylsterols (24-methylenecholesterol and episterol). Our results show that sterol composition is greatly modified during ontogeny of B. graminis conidia both at the qualitative and quantitative levels. In particular, 24-methylsterols, e.g., 24-methylenecholesterol and episterol, are the major sterols in old conidia whereas 24-ethylsterols, e.g., 24-ethylcholesta-5,22-dienol, 24-ethylcholesterol, and Δ5-avenasterol, are the main sterols in young conidia.Key words: Erysiphe, wheat powdery mildew, sterols, ontogeny.

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

1975 ◽  
Vol 53 (22) ◽  
pp. 2589-2597 ◽  
Author(s):  
H. H. Edwards
Keyword(s):  
Powdery Mildew ◽  
Host Cell ◽  
Electron Density ◽  
Epidermal Cells ◽  
Dense Material ◽  
Ultrastructural Changes ◽  
Electron Dense Material ◽  
Host Cytoplasm ◽  
Powdery Mildew Infection ◽  
Cell Protoplast

M1-a-mediated resistance in barley to invasion by the CR3 race of Erysiphe graminis 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: (1) 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 and are directly attributable to the gene M1-a. These changes are typical of stress or incompatibility responses and thus M1-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 M1-a.

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