Ecological genetics of an induced plant defense against herbivores: additive genetic variance and costs of phenotypic plasticity.

Adaptive phenotypic plasticity in chemical defense is thought to play a major role in plant-herbivore interactions. We investigated genetic variation for inducibility of defensive traits in wild radish plants and asked if the evolution of induction is constrained by costs of phenotypic plasticity. In a greenhouse experiment using paternal half-sibling families, we show additive genetic variation for plasticity in glucosinolate concentration. Genetic variation for glucosinolates was not detected in undamaged plants, but was significant following herbivory by a specialist herbivore, Pieris rapae. On average, damaged plants had 55% higher concentrations of glucosinolates compared to controls. In addition, we found significant narrow-sense heritabilities for leaf size, trichome number, flowering phenology, and lifetime fruit production. In a second experiment, we found evidence of genetic variation in induced plant resistance to P. rapae. Although overall there was little evidence for genetic correlations between the defensive and life-history traits we measured, we show that more plastic families had lower fitness than less plastic families in the absence of herbivory (i.e., evidence for genetic costs of plasticity). Thus, there is genetic variation for induction of defense in wild radish, and the evolution of inducibility may be constrained by costs of plasticity.

Spatial organization of the glucosinolate-myrosinase system in brassica specialist aphids is similar to that of the host plant.

Secondary metabolites are important in plant defence against pests and diseases. Similarly, insects can use plant secondary metabolites in defence and, in some cases, synthesize their own products. The paper describes how two specialist brassica feeders, Brevicoryne brassicae (cabbage aphid) and Lipaphis erysimi (turnip aphid) can sequester glucosinolates (thioglucosides) from their host plants, yet avoid the generation of toxic degradation products by compartmentalizing myrosinase (thioglucosidase) into crystalline microbodies. We propose that death, or damage, to the insect by predators or disease causes disruption of compartmentalized myrosinase, which results in the release of isothiocyanate that acts as a synergist for the alarm pheromone E-beta-farnesene.

Secondary metabolites in plant defence mechanisms.

Many secondary metabolites found in plants have a role in defence against herbivores, pests and pathogens. In this review, a few examples are described and discussed, and some of the problems in determining the precise role(s) of such metabolites highlighted. The role of secondary metabolites in defence may involve deterrence/anti-feedant activity, toxicity or acting as precursors to physical defence systems. Many specialist herbivores and pathogens do not merely circumvent the deterrent or toxic effects of secondary metabolites but actually utilize these compounds as either host recognition cues or nutrients (or both). This is true of both cyanogenic glucosides and glucosinolates, which art discussed in detail as examples of defensive compounds. Their biochemistry is compared and contrasted. An enormous variety of secondary metabolites are derived from shikimic acid or aromatic amino acids, many of which have important roles in defence mechanisms. Several classes of secondary products are 'induced' by infection, wounding or herbivory, and examples of these are given. Genetic variation in the speed and extent of such induction may account, at least in part, for the difference between resistant and susceptible varieties. Both salicylates and jasmonates have been implicated as signals in such responses and in many other physiological processes, though their prescise roles and interactions in signalling and development are not fully understood. Contents Summary 617 I. Introduction 617 II. Cyanogenic glucosides 618 III. Glucosinolates 619 IV. Non-protein amino acids 621 V. Alkaloids 622 VI. Plant phenoiics 623 VII. Plant terpenes, sesquiterpenoids and sterols 626 VIII. Phytoalexins 626 IX. Salicylic acid and methyl jasnionate 627 X. Conclusions 628 References 629.