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.
Highlights
Predicting the spread of soil-borne pathogens in the field would prove valuable for building efficient and sustainable strategies to limit crop damage
We investigated how host exploitation by a soilborne plant pathogen sustains its spread in soil based on a two-step process: infection of the host and subsequent exploitation of the infected host
We assumed that ontogenic resistance, defined as any change in resistance to pathogens correlated with the developmental stage of the host plant or its organs [23], would notably impact this two-step process
Summary
Predicting the spread of soil-borne pathogens in the field would prove valuable for building efficient and sustainable strategies to limit crop damage. Investigating variations in pathogen spreading rates over time and space constitutes an open research area. One of the determinants of pathogen spread is the access to nutrients [1], most pathogens finding resources solely in their host. The spread of soil-borne pathogens, such as Rhizoctonia solani, is driven by two types of resource: 1) organic matter, when the fungus acts as a saprotroph; 2) infected tissues of the host, when the fungus acts as a pathogen [2,3]. Pathogen ability to access and use organic matter has been extensively studied in the literature. Rich nutrient sources were shown to enhance saprotrophic growth
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