Abstract
Leptosphaeria maculans is a phytopathogenic fungus responsible for stem canker on Brassica napus. Its infectious cycle goes through an early phase of leaf infection and a late phase of colonisation and infection of the stem. The disease is mainly controlled by plant genetic resistances targeting a limited set of early fungal effector genes overexpressed during leaf infection and located in dynamic repeat-rich genomic regions. Thus, these resistances can be rapidly overcome by the pathogen. To find new sources of resistance, we focused on late effector genes, expressed during stem infection and located in gene-rich regions. A previous study revealed a quantitative resistance in the stem, partly relying on a gene-for-gene interaction with a late effector gene. In this study, we deciphered whether all late effector genes shared the same genomic and evolutionary characteristics and if they could be more stable than early effector genes, rendering the resistance they trigger more durable. In addition, as previous studies highlighted new criteria for selecting late effectors and suggested B. napus semi-winter genotypes as an interesting genetic pool for uncovering resistance sources, we selected six new late effector gene candidates and screened an enlarged panel of semi-winter genotypes. We revealed that early and late effector genes diverged for most of their genomic characteristics, supporting the hypothesis of late effector genes being more conserved. Moreover, we revealed new resistance sources to late effector genes, almost all belonging to the semi-winter genetic pool, validating their importance to uncover new resistance sources.