Abstract

Key Message Using disease bioassays and transcriptomic analysis we show that intact SA-signalling is required for potato defences against the necrotrophic fungal pathogenAlternaria solani. Early blight, caused by the necrotrophic fungusAlternaria solani,is an increasing problem in potato cultivation. Studies of the molecular components defining defence responses toA. solaniin potato are limited. Here, we investigate plant defence signalling with a focus on salicylic acid (SA) and jasmonic acid (JA) pathways in response toA. 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 ofArabidopsis thalianaagainst necrotrophic pathogens. We also present transcriptomic analysis with 36 arrays ofA. solaniinoculated 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-relatedgenes, 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 pathogenA. solani.

Keywords

Early blight; Alternaria solani; SA; JA; NahG; Coi1; Potato; Solanum tuberosum

Published in

Plant Molecular Biology
2020, volume: 104, number: 1, pages: 1-19
Publisher: SPRINGER

Authors' information