Plants produce a diverse array of secondary metabolites, many of which have antifungal activity. Some of these compounds are constitutive, existing in healthy plants in their biologically active forms. Others, such as cyanogenic glycosides and glucosinolates, occur as inactive precursors and are activated in response to tissue damage or pathogen attack. This activation often involves plant enzymes, which are released as a result of breakdown in cell integrity. Compounds belonging to the latter category are still regarded as constitutive because they are immediately derived from preexisting constituents (Mansfield, 1983). VanEtten et al. (i994) have proposed the term “phytoanticipin” to distinguish these preformed antimicrobial compounds from phytoalexins, which are synthesized from remote precursors in response to pathogen attack, probably as a result of de novo synthesis of enzymes. In recent years, studies of plant disease resistance mechanisms have tended to focus on phytoalexin biosynthesis and other active responses triggered after pathogen attack (Hammond-Kosack and Jones, 1996, in this issue). In contrast, preformed inhibitory compounds have received relatively little attention, despite the fact that these plant antibiotics are likely to represent one of the first chemical barriers to potential pathogens. The distribution of preformed inhibitors within plants is often tissue specific (e.g., Price et ai., 1987; Poulton, 1988; Davis, 1991; Fenwick et ai., 1992; Bennett and Wallsgrove, 1994), and r there is a tendency for these compounds to be concentrated in the outer cell layers of plant organs, suggesting that they may indeed act as deterrents to pathogens and pests. Some diffusible preformed inhibitors, such as catechol and protocatechuic acid (which are found in onion scales), may influence fungal growth at the plant surface. In general, however, preformed antifungal compounds are commonly sequestered in vacuoles or organelles in healthy plants. Therefore, the concentrations that are encountered by an invading fungus will depend on the extent to which that fungus causes tissue damage. Biotrophs may avoid the release of preformed inhibitors by minimizing damage to the host, whereas necrotrophs are likely to cause substantial release of these compounds. The nature and leve1 of preformed inhibitors to which a potential pathogen is exposed will also vary, depending on factors such as host genotype, age, and environmental conditions (Price et ai., 1987; Davis, 1991). There have been numerous attempts to associate natural variation in levels of preformed inhibitors in plants with resistance to particular pathogens, but often these attempts have failed to reveal any positive correlation. However, whereas preformed inhibitors may be effective against a broad spectrum of potential pathogens, successful pathogens are likely to be able to circumvent the effects of these antibiotics either by avoiding them altogether or by tolerating or detoxifying them (Schonbeck and Schlosser, 1976; Fry and Myers, 1981; Bennett and Wallsgrove, 1994; VanEtten et al., 1995; Osbourn, 1996). The isolation of plant mutants defective in the biosynthesis of preformed inhibitors would allow a direct genetic test of the importance of these compounds in plant defense. However, in most cases this approach is technically difficult because of the problems associated with screening for lossof the compounds. In the absence of plant mutants, a complementary approach involving the study of fungal mechanisms of resistance to preformed inhibitors, and of the contribution of this resistance to fungal pathogenicity to the relevant host plants, offers another route toward investigating the importance of these inhibitors in plant defense. A large number of constitutive plant compounds have been reported to have antifungal activity. Well-known examples include phenols and phenolic glycosides, unsaturated lactones, sulphur compounds, saponins, cyanogenic glycosides, and glucosinolates (reviewed in Ingham, 1973; Schonbeck and Schlosser, 1976; Fry and Myers, 1981; Mansfield, 1983; Ku6, 1992; Bennett and Wallsgrove, 1994; Grayer and Harborne, 1994; Osbourn, 1996). More recently, 5-alkylated resorcinols and dienes have been associated with disease resistance, in this case, resistance of subtropical fruits to infection by Collefotrichum gloeosporioides (Prusky and Keen, 1993). However, only a few classes of preformed inhibitor have been studied in detail to determine their possible roles in plant defense against fungal pathogens. This review focuses on three of these classes-saponins, cyanogenic glycosides, and glucosinolates-and summarizes our current knowledge of the role of these preformed inhibitors in determining the outcome of encounters between plants and phytopathogenic fungi.

Preformed Antimicrobial Compounds and Plant Defense against Fungal Attack.

Publisher Summary This chapter describes the advances with an emphasis on the structures of the alcohol dehydrogenases and the relationship between structure and function Yeast and mammalian alcohol dehydrogenase differ in substrate specificity and rate of catalytic activity The classic yeast enzyme is more specific for acetaldehyde and ethanol, which is consistent with its recognized physiological Significance to participate in alcohol fermentation at the end of the glycolytic pathway Enzyme forms with other functions and properties also occur in yeast The mammalian enzymes have broad substrate specificity and, even with primary alcohols, the maximum activity is not observed with ethanol Alcohols including ethanol, produced in the intestinal tracts mainly by bacterial actions, are found in the portal vein One physiological function of liver alcohol dehydrogenase may be to metabolize these products Structural studies have established that mammalian alcohol dehydrogenases have a distant evolutionary link to both the yeast and bacterial enzymes Ingested alcohol is metabolized to acetaldehyde mainly by the action of liver alcohol dehydrogenase

3 Alcohol Dehydrogenases

Many plants produce low-molecular-weight compounds which inhibit the growth of phytopathogenic fungi in vitro. These compounds may be preformed inhibitors that are present constitutively in healthy plants (also known as phytoanticipins), or they may be synthesized in response to pathogen attack (phytoalexins). Successful pathogens must be able to circumvent or overcome these antifungal defenses, and this review focuses on the significance of fungal resistance to plant antibiotics as a mechanism of pathogenesis. There is increasing evidence that resistance of fungal pathogens to plant antibiotics can be important for pathogenicity, at least for some fungus-plant interactions. This evidence has emerged largely from studies of fungal degradative enzymes and also from experiments in which plants with altered levels of antifungal secondary metabolites were generated. Whereas the emphasis to date has been on degradative mechanisms of resistance of phytopathogenic fungi to antifungal secondary metabolites, in the future we are likely to see a rapid expansion in our knowledge of alternative mechanisms of resistance. These may include membrane efflux systems of the kind associated with multidrug resistance and innate resistance due to insensitivity of the target site. The manipulation of plant biosynthetic pathways to give altered antibiotic profiles will also be valuable in telling us more about the significance of antifungal secondary metabolites for plant defense and clearly has great potential for enhancing disease resistance for commercial purposes.

Fungal Resistance to Plant Antibiotics as a Mechanism of Pathogenesis

Recent advances in the cell, developmental, and molecular biology of alkaloid biosynthesis have heightened our appreciation for the complexity and importance of plant secondary pathways. Several biosynthetic genes involved in the formation of tropane, benzylisoquinoline, and terpenoid indole alkaloids have now been isolated. The early events of signal perception, the pathways of signal transduction, and the function of gene promoters have been studied in relation to the regulation of alkaloid metabolism. Enzymes involved in alkaloid biosynthesis are associated with diverse subcellular compartments including the cytosol, vacuole, tonoplast membrane, endoplasmic reticulum, chloroplast stroma, thylakoid membranes, and perhaps unique "biosynthetic" or transport vesicles. Localization studies have shown that sequential alkaloid biosynthetic enzymes can also occur in distinct cell types, suggesting the intercellular transport of pathway intermediates. Isolated genes have also been used to genetically alter the accumulation of specific alkaloids and other plant secondary metabolites. Metabolic modifications include increased indole alkaloid levels, altered tropane alkaloid accumulation, elevated serotonin synthesis, reduced indole glucosinolate production, redirected shikimate metabolism, and increased cell wall-bound tyramine formation. This review discusses the biochemistry, cell biology, molecular regulation, and metabolic engineering of alkaloid biosynthesis in plants.

ALKALOID BIOSYNTHESIS IN PLANTS: Biochemistry, Cell Biology, Molecular Regulation, and Metabolic Engineering Applications.

Molecular activities, biosynthesis and evolution of triterpenoid saponins.

Saponins: Chemistry and Pharmacology of Natural Products By K. Hostettman and A. Marston (Lausanne University, Switzerland). Cambridge University Press: Cambridge, U.K. 1995. xii + 548 pp. $120.00. ISBN 0-521-32970-1.

George R. Waller

Papers

Saponins: Chemistry and Pharmacology of Natural Products By K. Hostettman and A. Marston (Lausanne University, Switzerland). Cambridge University Press: Cambridge, U.K. 1995. xii + 548 pp. $120.00. ISBN 0-521-32970-1.

Purine and purine alkaloid metabolism in Camellia and Coffea plants

Studies on the composition of the essential oils of three Nepeta species

Biosynthesis of the pyridine ring of ricinine.

Effect of Production Systems on Performance, Body Compostion and Lipid and Mineral Profiles of Soft Tissue in Cattle