Composition analysis of "halo" area of barley leaf epidermis induced by powdery mildew infection.

Powdery mildew (PM) caused by Blumeria graminis (DC.) Golovin ex Speer f. sp. hordei Marchal (Bgh) is one of the major yield reducing diseases in hulless barley (Hordeum vulgare L. var. nudum Hook. f.). Genotypes with contrasting resistance to PM offer unique opportunities to explore the transcriptome in order to understand the expression changes in genes and pathways. In this study, we explored the phytohormone levels and transcriptome of a Bgh susceptible (XL19) and resistant (ZYM1288) hulless barley genotypes at 0, 5, 12, 24, and 36 h post infection (hpi) with Bgh. We found relatively higher levels of abscisic acid, jasmonic acid, salicylic acid, and cytokinins in ZYM1288. The transcriptome analyses identified 31,354 genes that were enriched in signaling, energy, and defense related pathways. Higher numbers of differentially expressed genes (DEGs) were found in XL19 as compared to ZYM1288 after 5 (3603 vs. 2341) and 12 hpi (3530 vs. 2416). However, after 24 and 36 hpi, the number of DEGs was higher in ZYM1288 as compared to XL19 i.e., 3625 vs. 3034 and 5855 vs. 2725, respectively. Changes in hormone levels drove downstream expression changes in plant-hormone signaling that helped ZYM1288 to perform better under Bgh infection. The expression of DEGs in MAPK-signaling and Toll-like receptor signaling pathways, glucosinolate biosynthesis, glutathione metabolism, brassinosteroid metabolism, and energy related pathways indicated their common roles in defense against PM. Key genes related to PM-resistance were upregulated in the resistant genotype. These genes provide key information towards differences in both genotypes towards resistance to PM. The transcriptomic signatures explored in this study will broaden our understanding towards molecular regulation of resistance to PM in hulless barley.

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AtSTP8, an endoplasmic reticulum‐localized monosaccharide transporter from Arabidopsis , is recruited to the extrahaustorial membrane during powdery mildew infection

New Phytologist ◽

10.1111/nph.17347 ◽

2021 ◽

Author(s):

Jie Liu ◽

Mengxue Liu ◽

Liqiang Tan ◽

Baoyu Huai ◽

Xianfeng Ma ◽

...

Keyword(s):

Endoplasmic Reticulum ◽

Powdery Mildew ◽

Monosaccharide Transporter ◽

Powdery Mildew Infection

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

Canadian Journal of Botany ◽

10.1139/b75-286 ◽

1975 ◽

Vol 53 (22) ◽

pp. 2589-2597 ◽

Cited By ~ 10

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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