Interplay between Parasitism and Host Ontogenic Resistance in the Epidemiology of the Soil-Borne Plant Pathogen Rhizoctonia solani

Abstract

Spread of soil-borne fungal plant pathogens is mainly driven by the amount of resources the pathogen is able to capture and exploit should it behave either as a saprotroph or a parasite. Despite their importance in understanding the fungal spread in agricultural ecosystems, experimental data related to exploitation of infected host plants by the pathogen remain scarce. Using Rhizoctonia solani / Raphanus sativus as a model pathosystem, we have obtained evidence on the link between ontogenic resistance of a tuberizing host and (i) its susceptibility to the pathogen and (ii) after infection, the ability of the fungus to spread in soil. Based on a highly replicable experimental system, we first show that infection success strongly depends on the host phenological stage. The nature of the disease symptoms abruptly changes depending on whether infection occurred before or after host tuberization, switching from damping-off to necrosis respectively. Our investigations also demonstrate that fungal spread in soil still depends on the host phenological stage at the moment of infection. High, medium, or low spread occurred when infection was respectively before, during, or after the tuberization process. Implications for crop protection are discussed.

Reducing the Use of Pesticides with Site-Specific Application: The Chemical Control of Rhizoctonia solani as a Case of Study for the Management of Soil-Borne Diseases

“…Previous studies [ 33 , 37 ] have already reported that pathogenic spread is more extensive than saprotrophic spread. The exploitation of the resources of the infected host allows the fungus to sustain its spread through translocation processes.…”

“…It is known as a major soil-borne pathogen on several crops and causes various types of symptoms depending on host phenology at the time of infection, i.e. damping-off at early stages or necrosis and sclerotium formation later, particularly on tuberizing hosts [ 37 ]. Its spread in soil is sustained by organic matter (saprotrophic spread) or tissues of the infected host (pathogenic spread) through translocation processes [ 38 , 39 ].…”

Effect of Temperature on Growth and Development of Rhizoctonia solani (Kühn) f. sp. saskii Exner Incitant of Banded Leaf and Sheath Blight of Maize

“…Sclerotia which survive on plant debris often come up on the soil surface during field preparation and other operations. They come in contact with newly planted seedlings/plants and cause infection (Simon, 2014). Secondary spread is due to contact of healthy plants with infected leaves/sheaths and is responsible for the distribution of the pathogen during the main growing season of the crop (Gilligan, 2002).…”

Oomycete communities in lowland tropical forest soils vary in abundance and are composed of saprophytes and pathogens of seeds and seedlings of multiple plant species.

“…Damping off is often amplified at high seed and seedling densities because diseased individuals enhance both the growth and the dispersal of the pathogen via mycelia and zoospores. This results in an exponential rate of spore production, dispersal, and infection of nearby seeds and seedlings until seeds or seedlings are at densities sufficiently low or spaced at distances sufficiently large to limit dispersal (Burdon and Chilvers 1975, Augspurger and Kelly 1984) or grow and accrue resources to resist infection through ontogenic resistance (Simon et al 2014, Ampt et al 2022).…”