Key Message Using disease bioassays and transcriptomic analysis we show that intact SA-signalling is required for potato defences against the necrotrophic fungal pathogen Alternaria solani . Abstract Early blight, caused by the necrotrophic fungus Alternaria solani, is an increasing problem in potato cultivation. Studies of the molecular components defining defence responses to A. solani in potato are limited. Here, we investigate plant defence signalling with a focus on salicylic acid (SA) and jasmonic acid (JA) pathways in response to A. solani . Our bioassays revealed that SA is necessary to restrict pathogen growth and early blight symptom development in both potato foliage and tubers. This result is in contrast to the documented minimal role of SA in resistance of Arabidopsis thaliana against necrotrophic pathogens. We also present transcriptomic analysis with 36 arrays of A. solani inoculated SA-deficient, JA-insensitive, and wild type plant lines. A greater number of genes are differentially expressed in the SA-deficient mutant plant line compared to the wild type and JA- insensitive line. In wild type plants, genes encoding metal ion transporters, such as copper, iron and zinc transporters were upregulated and transferase-encoding genes, for example UDP-glucoronosyltransferase and Serine-glyoxylate transferase, were downregulated. The SA-deficient plants show upregulation of genes enriched in GO terms related to oxidoreductase activity, respiratory chain and other mitochondrial-related processes. Pathogenesis-related genes, such as genes encoding chitinases and PR1, are upregulated in both the SA-deficient and wild type plants, but not in the JA-insensitive mutants. The combination of our bioassays and the transcriptomic analysis indicate that intact SA signalling, and not JA signalling, is required for potato defences against the necrotrophic pathogen A. solani . Electronic supplementary material The online version of this article (10.1007/s11103-020-01019-6) contains supplementary material, which is available to authorized users.