Sclerotinia head rot (SHR), caused by the necrotrophic fungus Sclerotinia sclerotiorum, is one of the most devastating sunflower crop diseases. Despite its worldwide occurrence, the genetic determinants of plant resistance are still largely unknown. Here, we investigated the Sclerotiniasunflower pathosystem by analysing temporal changes in gene expression in one susceptible and two tolerant inbred lines (IL) inoculated with the pathogen under field conditions. Differential expression analysis showed little overlapping among ILs, suggesting genotype-specific control of cell defense responses possibly related to differences in disease resistance strategies. Functional enrichment assessments yielded a similar pattern. However, all three ILs altered the expression of genes involved in the cellular redox state and cell wall remodeling, in agreement with current knowledge about the initiation of plant immune responses. Remarkably, the over-representation of long non-coding RNAs (lncRNA) was another common feature among ILs. Our findings highlight the diversity of transcriptional responses to SHR within sunflower breeding lines and provide evidence of lncRNAs playing a significant role at early stages of defense. Sunflower is one of the most important crops for the production of high-quality oil and seeds consumed by both humans and livestock. In recent years, sunflower production showed a steady increase driven by a boost in sunflower oil consumption (FAO, 2017). However, the projected expansion of the sunflower oil market requires appropriate agronomic management and improved genetic resources to cope with abiotic and biotic stresses. Among the latter, special attention should be paid to fungal diseases, as they have the greatest impact on yield and seed quality 1. The necrotrophic fungus Sclerotinia sclerotiorum is the causal agent of Sclerotinia head (SHR) and stalk (SSR) rots in sunflower. In particular, SHR is a recurrent disease in sunflower-growing areas worldwide. It affects oil quality and, under favourable conditions, may lead to total production loss 1,2. Chemical fungicides proved to be ineffective and breeding of resistant genotypes has emerged as the most promising control strategy 3. So far, there is no evidence of any major gene controlling the resistance to SHR in sunflower. Instead, inbred lines (ILs) show a broad range of responses in accordance with quantitative disease resistance (QDR) patterns depending on the genotype 4-8. During the last 20 years, QTL mapping techniques have been used to unravel the complexity of the defense response to both SHR and SSR in sunflower. Biparental mapping has led to the discovery of several main effect loci and epistatic interactions 9-11 , whereas association mapping has served to identify candidate genes