Wagner Geoffrey

PhD defended june13, 2012
Direction: Régine Delourme & Maria Manzanares-Dauleux

Abstract

Clubroot is an expanding disease affecting Brassicaceae species, notably oilseed rape, Brassica napus L. Nowadays, disease control is achieved by the use of resistant varieties, under monogenic control, but overcoming of these resistances has been reported. The use of partial quantitative resistance could improve potential durability of clubroot resistance, with the underlying hypothesis that combining different mechanisms would slow down the adaptation of pathogen populations. In this context, the objective of this work was to decipher the mechanisms associated with clubroot partial quantitative resistance in oilseed rape.

We investigated (i) the metabolic changes induced after clubroot infection in oilseed rape with different level of resistance and (ii) the relationship between the genetic factors controlling the accumulation of metabolites in infected plants and QTL associated with clubroot resistance. We focused on Darmor-bzh, characterized by a high level of partial quantitative resistance, and for which histopathological analyses showed a high limitation of pathogen development from 21 days post inoculation. Focusing on the primary metabolism changes in response to clubroot infection, an accumulation of free amino acids in infected roots correlated to the level of symptoms was showed. This could be associated with the establishment of trophic relationships between the host and the pathogen. A targeted metabolic approach showed a depletion of indole glucosinolates in Darmor-bzh in the early steps of the secondary phase of the infection, which could contribute to symptom limitation through the decrease of auxin content in the plant. The functional genetic architecture was then investigated in the Darmor-bzh x Yudal DH progeny. Four main metabolic QTL hot-spots were highlighted, of which three colocalised with QTL for clubroot resistance, supporting thus the relationship between resistance and primary and secondary metabolites. Since different metabolic profiles underlie each hot-spot, resistant genotypes with different mechanisms can be designed for a better durability.