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Leaf rust induced volatile organic compounds signalling in willow during the infection

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Abstract

Plants are known to emit volatile organic compounds (VOC) in response to various biotic or abiotic stresses. Although the VOC emission in the case of insect attacks is well described, there is only little known about the impact of pathogens on plant emission. In the present study, we used a willow-leaf rust system to describe the effects of a biotrophic fungal infection on the VOC emission pattern of willow leaves. We detected that isoprene emissions from rust-infected leaves decreased threefold compared to control. The total monoterpene emissions did not change although a stress-signalling compound (Z)-β-ocimene showed an increase in infected plants on several days. The infection also increased the emission of sesquiterpenes and lipoxygenase products (LOX) by factors of 175-fold and 10-fold, respectively. The volatile emission signals showed two clear peaks during the experiment. At 6, 7 and 12 days post-infection (dpi), the relative volatile emission signal increased to about sixfold compared to uninfected plants. These time points are directly connected to rust infection since at 6 dpi the first rust pustules appeared on the leaves and at 12 dpi necrosis had developed around several pustules. We present correlations between LOX and sesquiterpene emission signals, which suggest at least two different steps in eliciting the volatile emission.

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Abbreviations

GC–MS:

Gas chromatography–mass spectrometry

LOX:

Lipoxygenase pathway products

MEP:

Methylerythritol phosphate pathway

MVP:

Mevalonate pathway

VOC:

Volatile organic compounds

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Acknowledgments

The financial support by the Estonian Science Foundation grants ETF 8110, JD101, SF1090065s07 and SF0170057s09 are gratefully acknowledged. We thank Gregory Heller for improving the English of our manuscript.

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Correspondence to Steffen M. Noe.

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Toome, M., Randjärv, P., Copolovici, L. et al. Leaf rust induced volatile organic compounds signalling in willow during the infection. Planta 232, 235–243 (2010). https://doi.org/10.1007/s00425-010-1169-y

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