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The infection processes of Sclerotinia sclerotiorum in cotyledon tissue of a resistant and a susceptible genotype of Brassica napus
- Garg, Harsh, Li, Hua, Sivasithamparam, Krishnapillai, Kuo, John, Barbetti, Martin J.
- Annals of botany 2010 v.106 no.6 pp. 897-908
- Brassica napus var. napus, Sclerotinia sclerotiorum, calcium oxalate, canola, cotyledons, crystals, cultivars, engineering, extrusion, genotype, host-pathogen relationships, hosts, hypersensitive response, leaves, mesophyll, microbial growth, pathogens, scanning electron microscopy, screening, starch, surface interactions
- BACKGROUND AND AIMS: Sclerotinia sclerotiorum can attack >400 plant species worldwide. Very few studies have investigated host-pathogen interactions at the plant surface and cellular level in resistant genotypes of oilseed rape/canola (Brassica napus). METHODS: Infection processes of S. sclerotiorum were examined on two B. napus genotypes, one resistant cultivar 'Charlton' and one susceptible 'RQ001-02M2' by light and scanning electron microscopy from 2 h to 8 d post-inoculation (dpi). KEY RESULTS: The resistant 'Charlton' impeded fungal growth at 1, 2 and 3 dpi, suppressed formation of appresoria and infection cushions, caused extrusion of protoplast from hyphal cells and produced a hypersensitive reaction. At 8 dpi, whilst in 'Charlton' pathogen invasion was mainly confined to the upper epidermis, in the susceptible 'RQ001-02M2', colonization up to the spongy mesophyll cells was evident. Calcium oxalate crystals were found in the upper epidermis and in palisade cells in susceptible 'RQ001-02M2' at 6 dpi, and throughout leaf tissues at 8 dpi. In resistant 'Charlton', crystals were not observed at 6 dpi, whereas at 8 dpi they were mainly confined to the upper epidermis. Starch deposits were also more prevalent in 'RQ001-02M2'. CONCLUSIONS: This study demonstrates for the first time at the cellular level that resistance to S. sclerotiorum in B. napus is a result of retardation of pathogen development, both on the plant surface and within host tissues. The resistance mechanisms identified in this study will be useful for engineering disease-resistant genotypes and for developing markers for screening for resistance against this pathogen.