Half of all insect species are dependent on living plant tissues, consuming about 10% of plant annual production in natural habitats and an even greater percentage in agricultural systems, despite sophisticated control measures. Plants are generally remarkably well-protected against insect attack, with the result that most insects are highly specialized feeders. The mechanisms underlying plant resistance to invading herbivores on the one side, and insect food specialization on the other, are the main subjects of this book. For insects these include food-plant selection and the complex sensory processes involved, with their implications for learning and nutritional physiology, as well as the endocrinological spects of life cycle synchronization with host plant phenology. In the case of plants exposed to insect herbivores, they include the activation of defence systems in order to minimize damage, as well as the emission of chemical signals that may attract natural enemies of the invading herbivores and maybe exploited by neighbouring plants that mount defences as well.

Insect-plant biology

Jasmonic acid and its derivatives can modulate aspects of fruit ripening, production of viable pollen, root growth, tendril coiling, and plant resistance to insects and pathogens. Jasmonate activates genes involved in pathogen and insect resistance, and genes encoding vegetative storage proteins, but represses genes encoding proteins involved in photosynthesis. Jasmonic acid is derived from linolenic acid, and most of the enzymes in the biosynthetic pathway have been extensively characterized. Modulation of lipoxygenase and allene oxide synthase gene expression in transgenic plants raises new questions about the compartmentation of the biosynthetic pathway and its regulation. The activation of jasmonic acid biosynthesis by cell wall elicitors, the peptide systemin, and other compounds will be related to the function of jasmonates in plants. Jasmonate modulates gene expression at the level of translation, RNA processing, and transcription. Promoter elements that mediate responses to jasmonate have been isolated. This review covers recent advances in our understanding of how jasmonate biosynthesis is regulated and relates this information to knowledge of jasmonate modulated gene expression.

Biosynthesis and action of jasmonates in plants

This paper examines induced resistance (SAR) in plants against various insect and pathogenic invaders. SAR confers quantitative protection against a broad spectrum of microorganisms in a manner comparable to immunization in mammals, although the underlying mechanisms differ. Discussed here are the molecular events underlying SAR: the mechanisms involved in SAR, including lignification and other structural barriers, pathogenesis-related proteins and their expression, and the signals for SAR including salicylic acid. Recent findings on the biological role of systemin, ethylene, jasmonates, and electrical signals are reviewed. Chemical activators of SAR comprise inorganic compounds, natural compounds, and synthetic compounds. Plants known to exhibit SAR and induced systemic resistance are listed.

Systemic acquired resistance

Wounding in multicellular eukaryotes results in marked changes in gene expression that contribute to tissue defense and repair. Using a cDNA microarray technique, we analyzed the timing, dynamics, and regulation of the expression of 150 genes in mechanically wounded leaves of Arabidopsis. Temporal accumulation of a group of transcripts was correlated with the appearance of oxylipin signals of the jasmonate family. Analysis of the coronatine-insensitive coi1-1 Arabidopsis mutant that is also insensitive to jasmonate allowed us to identify a large number of COI1-dependent and COI1-independent wound-inducible genes. Water stress was found to contribute to the regulation of an unexpectedly large fraction of these genes. Comparing the results of mechanical wounding with damage by feeding larvae of the cabbage butterfly (Pieris rapae) resulted in very different transcript profiles. One gene was specifically induced by insect feeding but not by wounding; moreover, there was a relative lack of water stress-induced gene expression during insect feeding. These results help reveal a feeding strategy of P. rapae that may minimize the activation of a subset of water stress-inducible, defense-related genes.

Differential Gene Expression in Response to Mechanical Wounding and Insect Feeding in Arabidopsis

The phytotoxin coronatine and the plant growth regulator methyl jasmonate (MeJA) caused similar growth-inhibitory effects on Arabidopsis seedlings. To test whether these two compounds have similar action, 14 independent coi1 (coronatine-insensitive) mutants of Arabidopsis were selected. The mutants segregated as single recessive Mendelian markers, and all were alleles at the coi1 locus. All coi1 mutants were also insensitive to MeJA and were male sterile. Both coronatine and MeJA inhibited root growth, stimulated anthocyanin accumulation, and increased the level of two proteins of ~31 and ~29 kD detected in SDS-polyacrylamide gels of wild-type Arabidopsis but caused none of these effects in the coi1 mutant. Coronatine and MeJA also induced the systemic appearance of proteinase inhibitor activity in tomato. The male-sterile flowers of the coi1 mutant produced abnormal pollen and had reduced level of an ~31-kD protein, which was abundant in the wild-type flowers. A coronatine-producing strain of Pseudomonas syringae grew in leaves of wild-type Arabidopsis to a population more than 100 times greater than it reached in the coi1 mutant. We conclude that coronatine mimics the action of MeJA and that coi1 controls a step in MeJA perception/response and in flower development.

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Arabidopsis Mutants Selected for Resistance to the Phytotoxin Coronatine Are Male Sterile, Insensitive to Methyl Jasmonate, and Resistant to a Bacterial Pathogen.

THE wound response of several plant species involves the activation of proteinase inhibitor (pin) genes and the accumulation of pin proteins at the local site of injury and systemically throughout the unwounded aerial regions of the plant1,2. It has been suggested that a mobile chemical signal is the causal agent linking the local wound stimulus to the distant systemic response, and candidates such as oligosaccharides3, abscisic acid4 and a polypeptide5,6 have been put forward. But the speed of transmission is high for the transport of a chemical signal in the phloem. The wound response of tomato plants can be inhibited by salicylic acid7 and agents like fusicoccin that affect ion transport8, and wounding by heat9 or physical injury produces electrical activity that has similarities to the epithelial conduction system10 used to transmit a stimulus in the defence responses of some lower animals11. Here we design experiments to distinguish between a phloem-transmissible chemical signal and a physically propagated signal based on electrical activity. We show that translocation in the phloem of tomato seedlings can be completely inhibited without effect on the systemic accumulation of pin transcripts and pin activity, and without hindrance to propagated electrical signals.

Electrical signalling and systemic proteinase inhibitor induction in the wounded plant

The electrical potential difference (E m ) across the plasma membrane of tomato leaf mesophyll cells consists of a cyanide-sensitive component, presumably produced by an H + -ATPase, and a cyanide-insensitive component. Variation of E m between different batches of tissue is mainly caused by variation in the cyanide-sensitive component. Oligogalacturonide elicitors that induce the synthesis of proteinase inhibitors in tomato seedlings depolarize the E m of tomato leaf mesophyll cells. This depolarization closely resembles that caused by cyanide: they are of similar magnitude and vary in a similar manner with variation in the initial E m of different batches of tissue. Treatments with cyanide and with the elicitors have similar effects on the small depolarization caused by KCl at 10 mol m −3 . The results suggest that the elicitors depolarize E m by inhibiting the plasma membrane H + -ATPase, but that the detailed mechanism of inhibition by the elicitors is different from that caused by cyanide

I. R. Gubb

Papers

Electrical signalling and systemic proteinase inhibitor induction in the wounded plant

Depolarization of tomato leaf cells by oligogalacturonide elicitors