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Hu, B.* ; Liu, Z.* ; Haensch, R.* ; Mithöfer, A.* ; Peters, F.S.* ; Vornam, B.* ; Messerer, M. ; Mayer, K.F.X. ; Wirén, N.* ; Rennenberg, H.*

Diplodia sapinea infection reprograms foliar traits of its pine (Pinus sylvestris L.) host to death.

Tree Physiol. 43, 611-629 (2022)
Postprint DOI PMC
Open Access Green
Infection with the necrotrophic fungus Diplodia sapinea is among the economically and ecologically most devastating diseases of conifers in the northern hemisphere accelerated by global climate change. The present study aims to characterize the changes mediated by D. sapinea infection on its pine host (Pinus sylvestris L.) that lead to the death of its needles. For this purpose, we performed an indoor infection experiment and inoculated shoot tips of pine seedlings with virulent D. sapinea. The consequences for foliar traits, including the phytohormone profile were characterized at both the metabolite and transcriptome level. Our results showed that D. sapinea infection strongly affected foliar levels of most phytohormones and impaired a multitude of other metabolic and structural foliar traits, such as ROS scavenging. Transcriptome analysis revealed that these changes are partially mediated via modified gene expression by fungal exposure. D. sapinea appears to overcome defense reactions of its pine host by reprogramming gene expression and post-transcriptional controls that determine essential foliar metabolic traits such as the phytohormone profile, cell wall composition and antioxidative system.
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Publication type Article: Journal article
Document type Scientific Article
Corresponding Author
Keywords Diplodia Sapinea Infection ; Ros Accumulation ; Anti-oxidative Metabolism ; Cellulose ; Chlorophyll ; Lignin ; Phytohormone Profile ; Transcriptome; Systemic Induced Resistance; Beech Fagus-sylvatica; Sphaeropsis-sapinea; Tip Blight; Antioxidative Metabolism; Phytohormone Profile; Defense Responses; Leaf Senescence; Gene-expression; Austrian Pine
ISSN (print) / ISBN 0829-318X
e-ISSN 1758-4469
Journal Tree Physiology
Quellenangaben Volume: 43, Issue: 4, Pages: 611-629 Article Number: , Supplement: ,
Publisher Oxford University Press
Publishing Place Great Clarendon St, Oxford Ox2 6dp, England
Non-patent literature Publications
Reviewing status Peer reviewed