Abstract

Jasmonate-mediated regulation of VOC emission has been extensively investigated in higher plants, however, only little is known about VOC production and its regulation in ferns. Here, we investigate whether the emission of VOCs from bracken fern Pteridium aquilinum is triggered by herbivory and if so - whether it is regulated by the octadecanoid signaling pathway. Interestingly, feeding of both generalist (Spodoptera littoralis) and specialist (Strongylogaster multifasciata) herbivores as well as application of singular and continuous mechanical wounding of fronds induced only very low levels of VOC emission. In contrast, treatment with jasmonic acid (JA) led to the emission of a blend of VOCs that was mainly comprised of terpenoids. Likewise, treatment with the JA precursor 12-oxo-phytodienoic acid (OPDA) and α-linolenic acid also induced VOC emission, albeit to a lower intesity than the JA treatment. Accumulation of endogenous JA was low in mechanically wounded fronds and these levels were unaffected by the application of oral secretions from both generalist or specialist herbivores. The emission of terpenoids upon JA treatment could be blocked with fosmidomycin and mevinolin, which are inhibitors of the MEP- and MVA pathways, respectively. These results indicate that similar to higher plants, terpenoid VOCs are produced via these pathways in bracken fern and that these pathways are JA-responsive. However, the very low amounts of terpenoids released after herbivory or mechanical damage are in stark contrast to what is known from higher plants. We speculate that S. multifasciata and S. littoralis feeding apparently did not induce the threshold levels of JA required for activating the MEP and MVA pathways and the subsequent volatile emission in bracken fern.

Highlights

  • The emission of volatile organic compounds (VOCs) is a wellknown indirect defence mechanism, by which plants recruit natural enemies of their herbivores [1], [2]

  • VOC emission after inhibitor treatment Since bracken produced both mono- and sesquiterpenes in response to jasmonic acid (JA) treatment, we investigated which metabolic pathways were involved in the production of these compounds using specific inhibitors

  • The basic questions why there is such a structural diversity of VOCs as well as how these evolved to function as an indirect defence mechanism in plants remain largely unanswered

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Summary

Introduction

The emission of volatile organic compounds (VOCs) is a wellknown indirect defence mechanism, by which plants recruit natural enemies (predators and parasitoids) of their herbivores [1], [2]. Terpenoids are the most abundant and structurally diverse class of VOCs that are released upon herbivore damage by many higher plants [4]. These can be a mixture of monoterpenes (C10), sesquiterpenes (C15), and homoterpenes (C11, C16), all of which are synthesized from a basic C5 unit, isopentenyl diphosphate (IPP) and dimethyallyl diphosphate (DMAPP) via either the cytosol-localized mevalonate (MVA) or plastid-localized methylerythritol (MEP) pathway [1], [4]. A huge body of literature is available on the regulation of VOC emission in many species of higher plant such as Phaseolus lunatus, Zea mays [5] Gossypium hirsutum [6], Populus simoniix, Nicotiana attenuata, and Solanum tuberosum [4], [7]. Very little is known about VOC emission in lower plants such as ferns (but see: [8], [9])

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