Damage-inducibility of primary and secondary metabolites in the wild parsnip (Pastinaca sativa)

Summary. Induction of secondary metabolites to herbivore damage is a widespread phenomenon among plants and serves to enhance resistance by reducing suitability or increasing toxicity of foliage. Post-damage responses of primary metabolites are less well known; reductions in primary metabolites may increase resistance by decreasing palatability or nutritional suitability for herbivores or by potentiating toxicity of secondary metabolites. In this study, we examined response to simulated herbivory in Pastinaca sativa, the wild parsnip, in both primary and secondary metabolites. We found that induction of secondary metabolites in response to damage is largely restricted to a single class of compounds, the furanocoumarins. These prooxidant compounds are known to be toxic to a wide variety of insect herbivores. The only primary metabolite that responded to damage was total soluble protein, which increased significantly 24 h after damage. After 24 h, the correlation between total furanocoumarins and total sugars was significant and negative (r = − 0.697). This correlation likely reflects an independent response of sugar to damage, rather than a diversion of resources into furanocoumarin production, inasmuch as this correlation at 3 h, after furanocoumarin induction had taken place, was not significant. In other secondary metabolite pathways, damage produced a significant decline in farnesene and a C-16 unsaturated fatty acid, 7,10,13-hexadecatrienoic acid, each of which may potentiate the furanocoumarin defense response. Farnesene may enhance photooxidative activation of the furanocoumarins and 7,10,13-hexadecatrienoic acid may serve as a precursor to jasmonic acid, a key hormone in regulating induction responses. With few key exceptions, quantities of both primary and secondary metabolites in wild parsnip foliage are unaffected by damage. Those that are affected may well play a role in resistance of parsnips to herbivores. Received 1 July 1998; accepted 28 September 1998.