ASSBT Biennial Meeting – Feb. 24 – Feb 27, 2025 in Long Beach, CA
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Histopathology of Rhizoctonia solani AG 2-2 infection of sugar beet.


The infection process for Rhizoctonia solani AG 2-2 was investigated by Ruppel in 1973, with two early resistant and two susceptible germplasm. Since that time, there have been advances in microscopy and detection methods. The aim of this work was to use advanced microscopy and detection methods to reexamine infection processes in sugar beet, evaluate the response of a modern resistant (highly resistant) and a susceptible germplasm, and to compare those responses with observations made in the 1970s. As in Ruppel’s work, infection on the root tissue occurred via infection cushions, but the presence of infection cushions was not always evident and direct penetration without forming an infection cushion is likely. Fungal hyphae that entered through the root surface were largely restricted to the outermost cortical layer in both the resistant and sensitive varieties. The outermost cambial ring appeared to act as a barrier to fungal progression, with hyphae invading only through breaks in the cambial ring where non-vascular tissue was present. However, within the root groove, fungal hyphae were observed that had entered, evidently by direct penetration, the tissues where feeder roots emerged. This infection strategy allowed deeper penetration of the fungus into the root, bypassing the potential barrier presented by the outermost cambium. As reported by Ruppel, symptoms were found in advance of the fungal hyphae. Observations of necrosis were consistent with a breakdown of plant tissue by fungal polygalacturonases. Increased affinity for propidium iodide in the area surrounding the invading hyphae indicated possible de-esterification of the cell walls, which may be a precursor to degradation by pectinases. Results did not support a lysis of fungal tissue as hypothesized by Ruppel. Instead, plant physical and chemical barriers were evident.