Abstract
Norway spruce (Picea abies) is an economically and ecologically important tree species that grows across northern and central Europe. Treating Norway spruce with jasmonate has long‐lasting beneficial effects on tree resistance to damaging pests, such as the European spruce bark beetle Ips typographus and its fungal associates. The (epi)genetic mechanisms involved in such long‐lasting jasmonate induced resistance (IR) have gained much recent interest but remain largely unknown. In this study, we treated 2‐year‐old spruce seedlings with methyl jasmonate (MeJA) and challenged them with the I. typographus vectored necrotrophic fungus Grosmannia penicillata. MeJA treatment reduced the extent of necrotic lesions in the bark 8 weeks after infection and thus elicited long‐term IR against the fungus. The transcriptional response of spruce bark to MeJA treatment was analysed over a 4‐week time course using mRNA‐seq. This analysis provided evidence that MeJA treatment induced a transient upregulation of jasmonic acid, salicylic acid and ethylene biosynthesis genes and downstream signalling genes. Our data also suggests that defence‐related genes are induced while genes related to growth are repressed by methyl jasmonate treatment. These results provide new clues about the potential underpinning mechanisms and costs associated with long‐term MeJA‐IR in Norway spruce.
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