Julie NOAH's thesis defense

The jury was composed of :

Daniel CROLL, Professeur des universités, Université de Neuchâtel                        Rapporteur & Examinateur
Laurence GODIARD, Chargée de recherche, INRAE, Université de Toulouse         Rapporteure & Examinatrice
Maël BAUDIN, Professeur junior, INRAE, Université d’Angers                                      Examinateur
Marie DUFRESNE, Professeure des universités, Université Paris Saclay                   Examinatrice
Fanny HARTMANN, Maîtresse de conférence, CNRS, Université Paris Saclay         Invitée

Abstract: Leptosphaeria maculans is a plant pathogenic fungus responsible for stem canker in crucifers and mainly in oilseed rape (Brassica napus). The favoured method to control this fungus is to select for monogenic resistances and introgress them into oilseed rape varieties used in the field. However, L. maculans is highly adaptable and can overcome monogenic resistance in cultivated varieties in just a few years. In this context, it is necessary to find new sources of resistance that would be more durable than the monogenic resistances currently used. To this end, we are interested in Brassica carinata (Ethiopian mustard), a species that is genetically close to B. napus and which shows extreme resistance to L. maculans. The aim of my PhD thesis is to determine the mechanisms by which L. maculans adapts to different Brassica species. To do this, it was necessary to characterize the status of B. carinata in relation to L. maculans. We were able to determine B. carinata as a nonhost species of L. maculans, but we also identified a few natural isolates capable of moderately infecting this species (better adaptation of these isolates than the average of L. maculans isolates infecting B. carinata). Using this biological material, I was able to identify genomic regions in L. maculans involved in adaptation to B. napus and B. carinata. Four QTL for adaptation to B. napus and three QTL for adaptation to B. carinata were identified in L. maculans, and a study of the genes present in these QTL intervals was carried out. Finally, I carried out a comparative transcriptomics analysis combined with cytology analyses, which enabled me to identify genes specifically expressed during infection in one or other of these two plant species and to characterize the infection processes during adapted and non-adapted interactions. This work has enabled us to highlight the different mechanisms by which L. maculans adapts to different hosts and has also revealed the emergence risks of strains newly adapted to species that are highly resistant.