Histopathology of Rhizoctonia root and crown rot of sugar beet reveals differential responses in susceptible and resistant cultivars to invasion by Rhizoctonia solani AG 2-2
Abstract
Background and Aims: Rhizoctonia solani AG 2-2 causes Rhizoctonia root and crown rot (RRCR) of sugar beet and is a major constraint on production worldwide. Sugar beet roots possess distinctive anatomical features, including a corky periderm, a root groove region and concentric vascular rings, which may influence infection outcomes. Adult-plant resistance is known but the mechanisms are unknown. This study provides an updated histopathology of RRCR and compares responses in resistant and susceptible varieties.
Methods: Six-week-old roots of susceptible (C869) and resistant (SR98/2) varieties were inoculated with R. solani AG 2-2 and sampled 2–12 d after inoculation. Tissue sections were examined using brightfield, epi-illumination, fluorescence and confocal microscopy. Stains included aniline blue, wheat germ agglutinin–Alexa Fluor 488, and pectin-specific antibodies LM19 and LM20. Hyphal penetration, infection cushion formation, tissue maceration and cell wall modifications were assessed.
Key Results: Unlike reports from other hosts, hyphae did not align with anticlinal walls or produce T-shaped branches but formed infection cushions through spur branching. Direct penetration occurred without cushions and was reduced on the resistant variety. Hyphae spread laterally between the periderm and outer cambium, with deeper penetration occurring where the outer cambium was disrupted. Tissues within the root groove were associated with structural discontinuities and were especially susceptible. Lesions could be delimited by the presence of red autofluorescence and, in the resistant variety, were bordered by callose. The susceptible variety showed loss of LM19/LM20 epitopes, indicating degradation of methylated and demethylated pectin. Resistant roots retained more LM19/LM20 signal, indicating reduced pectin degradation.
Conclusions: Early infection success is shaped by root anatomy, particularly outer cambium continuity and structures of the root groove. Resistant roots mounted a callose-associated response, whereas susceptible roots exhibited limited cell wall reinforcement. These findings refine the histopathology of RRCR and highlight potential targets for resistance breeding.
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BibTeX
@article{minier2026histopathology,
title = {{Histopathology of Rhizoctonia root and crown rot of sugar beet reveals differential responses in susceptible and resistant cultivars to invasion by Rhizoctonia solani AG 2-2}},
author = {Douglas H Minier and Linda E Hanson},
journal = {Annals of Botany},
year = {2026},
month = jul,
doi = {10.1093/aob/mcag201},
url = {https://doi.org/10.1093/aob/mcag201},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Histopathology of Rhizoctonia root and crown rot of sugar beet reveals differential responses in susceptible and resistant cultivars to invasion by Rhizoctonia solani AG 2-2
AU - Douglas H Minier
AU - Linda E Hanson
PY - 2026
DA - 2026/07/08
JO - Annals of Botany
DO - 10.1093/aob/mcag201
UR - https://doi.org/10.1093/aob/mcag201
AB - Background and Aims: Rhizoctonia solani AG 2-2 causes Rhizoctonia root and crown rot (RRCR) of sugar beet and is a major constraint on production worldwide. Sugar beet roots possess distinctive anatomical features, including a corky periderm, a root groove region and concentric vascular rings, which may influence infection outcomes. Adult-plant resistance is known but the mechanisms are unknown. This study provides an updated histopathology of RRCR and compares responses in resistant and susceptible varieties. Methods: Six-week-old roots of susceptible (C869) and resistant (SR98/2) varieties were inoculated with R. solani AG 2-2 and sampled 2–12 d after inoculation. Tissue sections were examined using brightfield, epi-illumination, fluorescence and confocal microscopy. Stains included aniline blue, wheat germ agglutinin–Alexa Fluor 488, and pectin-specific antibodies LM19 and LM20. Hyphal penetration, infection cushion formation, tissue maceration and cell wall modifications were assessed. Key Results: Unlike reports from other hosts, hyphae did not align with anticlinal walls or produce T-shaped branches but formed infection cushions through spur branching. Direct penetration occurred without cushions and was reduced on the resistant variety. Hyphae spread laterally between the periderm and outer cambium, with deeper penetration occurring where the outer cambium was disrupted. Tissues within the root groove were associated with structural discontinuities and were especially susceptible. Lesions could be delimited by the presence of red autofluorescence and, in the resistant variety, were bordered by callose. The susceptible variety showed loss of LM19/LM20 epitopes, indicating degradation of methylated and demethylated pectin. Resistant roots retained more LM19/LM20 signal, indicating reduced pectin degradation. Conclusions: Early infection success is shaped by root anatomy, particularly outer cambium continuity and structures of the root groove. Resistant roots mounted a callose-associated response, whereas susceptible roots exhibited limited cell wall reinforcement. These findings refine the histopathology of RRCR and highlight potential targets for resistance breeding.
SN - 0305-7364
SN - 1095-8290
ER -