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Research article2015Peer reviewed

Transcriptional responses of Norway spruce (Picea abies) inner sapwood against Heterobasidion parviporum

Oliva Palau, Jonàs; Rommel, S; Fossdal, C.G.; Hietala, A.M.; Nemesio Gorriz, Miguel; Solheim, H.; Elfstrand, Malin

Abstract

The white- rot fungus Heterobasidion parviporum Niemela & Korhonen establishes a necrotrophic interaction with Norway spruce ( Picea abies ( L.) H. Karst.) causing root and butt rot and growth losses in living trees. The interaction occurs first with the bark and the outer sapwood, as the pathogen enters the tree via wounds or root- to- root contacts. Later, when the fungus reaches the heartwood, it spreads therein creating a decay column, and the interaction mainly occurs in the inner sapwood where the tree creates a reaction zone. While bark and outer sapwood interactions are well studied, little is known about the nature of the transcriptional responses leading to the creation of a reaction zone. In this study, we sampled bark and sapwood both proximal and distal to the reaction zone in artificially inoculated and naturally infected trees. We quantified gene expression levels of candidate genes in secondary metabolite, hormone biosynthesis and signalling pathways using quantitative polymerase chain reaction. An up- regulation of mainly the phenylpropanoid pathway and jasmonic acid biosynthesis was found at the inoculation site, when inoculations were compared with wounding. We found that transcriptional responses in inner sapwood were similar to those reported upon infection through the bark. Our data suggest that the defence mechanism is induced due to direct fungal contact irrespective of the tissue type. Understanding the nature of these interactions is important when considering tree breeding- based resistance strategies to reduce the spread of the pathogen between and within trees.

Keywords

defence; forest pathogen; induced defence; necrotroph; reaction zone

Published in

Tree Physiology
2015, Volume: 35, number: 9, pages: 1007-1015
Publisher: OXFORD UNIV PRESS