Plants are constantly being challenged by aspiring pathogens, but disease is rare. Why? Broadly, there are three reasons for pathogen failure. Either (1) the plant is unable to support the niche requirements of a potential pathogen and is thus a non? host; or (2) the plant possesses preformed structural barriers or toxic compounds that confine successful infections to specialized pathogen species; or (3) upon recognition of the attacking pathogen, defense mechanisms are elaborated and the invasion remains localized. All three types of interaction are said to be incompatible, but only the latter resistance mech? anism depends on induced responses. Successful pathogen invasion and disease (compatibility) ensue if the preformed plant defenses are inappropriate, the plant does not detect the pathogen, or the activated defense responses are ineffective. In this review, we examine the essential prerequisites for patho? gen recognition and the induction of localized defense responses. Preformed defenses are considered elsewhere in this issue (see Osbourn, 1996, in this issue). Race-specific pathogen recognition is hypothesized to re? sult from the direct or indirect interaction of the product of a dominant or semidominant plant resistance (R) gene with a product derived from the corresponding dominant pathogen avirulence (Avr) gene (Keen, 1992; Staskawicz et al., 1995). Subsequent signal transduction events are assumed to coordinate the activation of an array of defense responses. This "simple" model appears to explain much but begs many questions. For example, R gene products are likely to provide key components for recognition, but how do the distinct classes of R proteins characterized to date (see Bent, 1996, in this is? sue) activate the defense response? Do different R gene classes activate distinct responses? The regulation of some components of defense mechanisms has been studied in plant cell cultures in response to non-race-specific elicitors, but to what extent do such studies provide a model for R gene func? tion? Plant resistance is often correlated with the activation of specific defense responses, but which (if any) are required to abolish or retard pathogen growth, and how? Which are pri? mary responses and which are secondary? Does the first response involve transcriptional regulation, the activation of preformed enzymes, and/or the opening of ion channels, or

Resistance gene-dependent plant defense responses.

Antibiotic phenols have been found in all plants investigated to date. Some occur constitutively and are thought to function as preformed inhibitors associated with nonhost resistance (84, 94, 128, 134). Others, which are the subject of this review, are formed in response to the ingress of pathogens, and their appearance is considered as part of an active defense response. Since the first suggestions that phenolic intermediates have a role in the active expres­ sion of resistance, an underlying problem in ascertaining that such secondary metabolites are of primary (rather than secondary) importance has been the localization and timing of the host response. In this review we address the problem of response localization and localization of phenolics relative to the sequential development of stages of disease that lead ultimately to resistance expression. Initial demonstrations that phenols are significant components of the host

Phenolic Compounds and Their Role in Disease Resistance

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

Lignin is a polymer of phenylpropanoid compounds formed through a complex biosynthesis route, represented by a metabolic grid for which most of the genes involved have been sequenced in several plants, mainly in the model-plants Arabidopsis thaliana and Populus. Plants are exposed to different stresses, which may change lignin content and composition. In many cases, particularly for plant-microbe interactions, this has been suggested as defence responses of plants to the stress. Thus, understanding how a stressor modulates expression of the genes related with lignin biosynthesis may allow us to develop study-models to increase our knowledge on the metabolic control of lignin deposition in the cell wall. This review focuses on recent literature reporting on the main types of abiotic and biotic stresses that alter the biosynthesis of lignin in plants.

https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1744-7909.2010.00892.x

Abiotic and Biotic Stresses and Changes in the Lignin Content and Composition in Plants

Infection of plants with pathogens like viruses or fungi often leads to a response of the host ranging from very mild to very severe. A very mild response usually does not result in considerable changes in the patterns of gene expression of the plant. However, a hypersensitive reaction, e.g., in the case of infection of Samsun NN tobacco with tobacco mosaic virus, is accompanied by a massive increase in the amounts of a large number of different proteins. Among these induced proteins are members of a group of so‐called pathogenesis‐related (PR) proteins. Frequently, the hypersensitively reacting host becomes resistant to subsequent pathogenic attack. The correlation of this phenomenon of acquired resistance and the induced protein synthesis suggests a direct involvement of these proteins in the observed replication deficiency of the pathogen. This has initiated studies by several research groups toward a better understanding of the role of these PR‐proteins in the hypersensitively reacting plant....

Pathogenesis-related proteins of plants

When highly resistant wheat (Triticum aestivum L.) varieties are infected by an avirulent race of the stem rust fungus (Puccinia graminis Pers. f. sp. tritici Erics. and E. Henn.), penetrated host cells undergo rapid necrotization. This hypersensitive cell death is correlated with cellular lignification which efficiently restricts further fungal growth. Three competitive inhibitors of phenylalanine ammonia-lyase, the first enzyme of the general phenylpropanoid pathway and, thus, of lignin biosynthesis, namely α-aminooxyacetate, α-aminooxy-β-phenylpropionic acid, and (1-amino-2-phenylethyl)phosphonic acid, and two highly specific irreversible suicide inhibitors of the lignification-specific enzyme cinnamyl-alcohol dehydrogenase, namely N(O-aminophenyl)sulfinamoyl-tertiobutyl acetate and N(O-hydroxyphenyl)sulfinamoyl-tertiobutyl acetate, were applied to genetically resistant wheat plants prior to inoculation with stem rust. Treatment with any of these inhibitors decreased the frequency of lignified necrotic host cells and concomitantly led to increased fungal growth. The cinnamyl-alcohol dehydrogenase inhibitors were generally more effective than the phenylalanine ammonia-lyase inhibitors, occasionally allowing some sporulation to occur on the resistant wheat leaves. These results clearly point to a causal relationship between the formation of lignin precursors and the resistance of wheat to stem rust.

Specific Inhibition of Lignification Breaks Hypersensitive Resistance of Wheat to Stem Rust

Whenhighly resistant wheat(Triticum aestivum L.)varieties areinfected byanavirulent raceofthestemrust fungus (Puccinia graminis Pers. f.sp.tritici Erics. andE.Henn.), penetrated host cells undergo rapid necrotization. Thishypersensitive cell death iscorrelated withcellular lignification whichefficiently restricts further fungal growth. Threecompetitive inhibitors ofphenylalanineammonia-lyase, thefirst enzymeofthegeneral phenylpropanoid pathway and,thus, oflignin biosynthesis, namely a-aminooxyacetate, a-aminooxy-B-phenylpropionic acid, and(1-amino2-phenylethyl)phosphonic acid, andtwohighly specific irreversiblesuicide inhibitors ofthelignification-sp ecific enzymecinnamyl-alcohol dehydrogenase, namelyN(O-aminophenyl)sulfinamoyl-tertiobutyl acetateandN(O-hydroxyphenyl)sulfinamoyltertiobutyl acetate, wereapplied togenetically resistant wheat plants prior toinoculation withstemrust. Treatment withanyof theseinhibitors decreased thefrequency oflignified necrotic host cells andconcomitantly ledtoincreased fungal growth. The cinnamyl-alcohol dehydrogenase inhibitors weregenerally more effective thanthephenylalanine ammonia-lyase inhibitors, occasionally allowing somesporulation tooccurontheresistant wheat leaves. Theseresults clearly point toacausal relationship betweentheformation oflignin precursors andtheresistance of wheattostemrust.

Liliane Gorrichon

Papers

Specific Inhibition of Lignification Breaks Hypersensitive Resistance of Wheat to Stem Rust

Specific Inhibition ofLignification BreaksHypersensitive Resistance ofWheattoStemRust