Lapous, R.; Haquet, C.; Denance, C.; Benejam, J.; Perchepied, L.; Hellyn, K.; Muranty, H.; Durel, C.-E.; Ferreira de Carvalho, J.

Apple scab, caused by Venturia inaequalis, remains one of the most damaging diseases in apple orchards, driving intensive pesticide use worldwide. Reducing this dependence requires the deployment of durable resistance, ideally through the combination of major resistance genes (R genes) with quantitative trait loci (QTL) that confer partial and potentially complementary protection. Yet, few apple scab QTLs have been functionally validated, and their underlying mechanisms remain largely unresolved. Here, we refined and functionally described, with transcriptomic data, five resistance QTLs in a biparental population of 1,970 individuals derived from the cross TN 10-8 x Fiesta. Using 43 newly developed KASP markers, QTL locations were substantially precised through high-resolution genotyping and phenotyping with two V. inaequalis isolates exhibiting contrasting virulence. Four QTLs (qT1, qF11, qF17, qT13) were validated, while qF3 was not confirmed. Transcriptomic data comparison revealed the expression of candidate genes within the narrowed intervals, including receptor-like proteins in qT1, and RNAi- and signaling-related genes in qF11 and qF17, suggesting a diversified and complementary defense network. These findings refine the genetic architecture of apple scab resistance and suppose the existence of shared molecular pathways between major R gene, such as the well-described Rvi6 gene, and quantitative resistance, with for instance the QTL qT1. The identified loci and markers provide robust tools for marker-assisted and genomic breeding aimed at developing apple cultivars with complementary and potentially durable resistance pathways.