Histopathology of Sclerotinia sclerotiorum infection and oxalic acid function in susceptible and resistant soybean. (31st March 2016)

• Record Type: Journal Article
• Authors: Davidson, A. L.; Blahut‐Beatty, L.; Itaya, A.; Zhang, Y.; Zheng, S.; Simmonds, D.
• Is Part Of: Plant pathology. Volume 65:Number 6(2016)
• Page Start: 878
• Page End: 887
• Publication Date: 2016-03-31
• Subjects: histopathology -- necrotroph -- oxalate oxidase -- oxalic acid -- Sclerotinia sclerotiorum -- soybean; Agricultural pests -- Periodicals; Plant diseases -- Periodicals; 632
• DOI: 10.1111/ppa.12514
• Languages: English
• ISSNs: 0032-0862

Abstract

Abstract : The success of the necrotrophic fungus Sclerotinia sclerotiorum is largely dependent on its major virulence factor, oxalic acid (OA). Virulence is lost in transgenic plants that express OA degrading enzymes, e.g. oxalate oxidase (OxO). The histopathology of S . sclerotiorum infection and OA accumulation was examined in a transgenic soybean line over‐expressing OxO (OxO‐OE) and its isogenic parent (WT). In situ flower inoculation showed that the OxO‐OE plants were highly resistant to the pathogen while the WT parents were susceptible. This difference in resistance was not apparent in the floral tissues, as aggressive hyphal activity was similar on both hosts, showing that high OxO activity and low OA accumulation in OxO‐OE was not a deterrent. However, the process of fungal infection on excised leaf tissue differed on the two hosts. Primary lesions developed and showed similar severe ultrastructural damage on both hosts but rapid lesion expansion (colonization) proceeded only on the WT, concomitant with OA accumulation. Oxalic acid rose in OxO‐OE 1 day post‐inoculation and did not change over the following 3 days, showing that colonization can be blocked by maintaining low levels of OA. However, OxO degradation of OA did not deter initial host penetration and primary lesion formation. This shows that OA, the major virulence factor of S. sclerotiorum, is critical for host colonization but may not be required during primary lesion formation, suggesting that other factors are contributing to the establishment of the primary lesion.