Abstract
The objective of the present study was to investigate to what extent the macroscopic phenotype of incompatible host-pathogen interactions reflects differences in fungal development and host responses at the histological level. This was done by conventional and advanced microscopic analysis of six wheat near-isogenic lines differing by individual R genes and inoculated with an avirulent isolate of Puccinia striiformis. Wheat line AvocetYr15 had the lowest macroscopic infection type (IT) 0-1, in which fungal growth was stopped at early stages due to extensive expression of a hypersensitive response (HR) at all time points (4, 8 and 16 days post-inoculation, dpi) without any sign of haustorial bodies. AvocetYr5 and AvocetYr1 had IT 1, in which most fungal colonies developed secondary hyphae. Many colonies were encased by HR at 16 dpi, more extensively in AvocetYr1 than AvocetYr5. In AvocetYr6 (IT 2), HR was expressed after the formation of secondary hyphae at 4 dpi, after which fungal growth and HR increased simultaneously until most colonies became encased by HR. AvocetYr27 (IT 2-3) and AvocetYr17 (IT 4-5) showed similar fungal growth and HR at 4 dpi, where HR was only weakly expressed in a few host cells. Encasement of secondary and runner hyphae increased significantly in AvocetYr27, but at 16 dpi, HR was often circumvented by large, intermingled fungal colonies in both lines. No resistance responses were observed in Avocet S (susceptible control). The very different histological patterns conferred by the six R genes suggests differences in the timing of the host-pathogen recognition and onset of host defence pathways.
Original language | English |
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Journal | Plant Pathology |
Volume | 68 |
Issue | 7 |
Pages (from-to) | 1320-1330 |
Number of pages | 11 |
ISSN | 0032-0862 |
DOIs | |
Publication status | Published - Sept 2019 |
Keywords
- histopathology
- hypersensitive response
- microscopy
- Puccinia striiformis
- R gene
- STRIIFORMIS F.SP TRITICI
- F-SP TRITICI
- PUCCINIA-STRIIFORMIS
- CELL-DEATH
- LOCALIZATION
- MECHANISMS
- CALLOSE
- CLONING
- GUARD