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

Abstract

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...

Quantitative Analysis of the Early Powdery Mildew Infection Stages on Resistant Barley Genotypes

“…Host cell collapse is likely to be involved at these stages. This has been reported to occur by BUSHNELL 1981, BUSHNELL and BERGQUIST 1975, EDWARDS 1975, JOHNSON et al 1979, MCKEEN and BHATTACHARYA 1970 and-al2 suggested that the genes in this group are triggered later, or perhaps to a different extent, or by a different mechanism. The variation suggests that there are differences in mechanism between the genes in group B, despite the fact that they develop the same infection type with CR3.…”

“…lines with the genes Ml-a, --a6, -a9 and -al3 reduced the fungal population by 98 % at the penetration stage. This has been reported to occur by BUSHNELL 1981, BUSHNELL and BERGQUIST 1975, EDWARDS 1975, JOHNSON et al 1979, MCKEEN and BHATTACHARYA 1970and ZEYEN and BUSHNELL 1979, all working on Ml-a, STANBRIDGE et al 1971working on Ml-a6, KOGA et al 1978, KOGA et al 1980and KOGA et al 1983 working on Ml-a9. Events occurring after ESH formation must be post-penetration events, as ESH has been shown to depend on a functional haustorium (ELLINGBOE 1972).…”

“…The most marked effect is the formation of a cell wall apposition (papilla), which prevents or counteracts penetration (BUSHNELL 1981, EDWARDS 1975, JOHNSON et al 1979, ZEYEN and BUSHNELL 1979). The work has been concentrated on a few resistance genes, primarily Ml-a.…”

“…The effect of this gene is not however, limited to a single mechanism. The most marked effect is the formation of a cell wall apposition (papilla), which prevents or counteracts penetration (BUSHNELL 1981, EDWARDS 1975, JOHNSON et al 1979, ZEYEN and BUSHNELL 1979). Other effects are the collapse of host cells (BUSHNELL 1981, EDWARDS 1975, JOHNSON et al 1979, ZEYEN and BUSHNELL 1979), delayed haustorial development (MASRI and ELLINGBOE 1966), reduced haustorial size (MASRI and ELLINGBOE 1966), malformation of haustoria (MASRI and ELLINGBOE 1966) and prevention of sporulation (MASRI and ELLINGBOE 1966, MCKEEN and BHATTACHARYA 1970).…”

Microscopical studies of resistance to powdery mildew disease in the hop cultivar Wye Target

“…Hypersensitive cell death has also been implicated in examples of race-specific resistanee to £. ^I,' /7//>//VN' .V in barley (Masri & EUingboe, 1966;McCoy & EUingboe, 1966;Edwards, 1975;Bushnell. 1981), in wheat (EUingboe, 1972Hyde & Colhoun, 1975) and in oats (Carver &.…”