Plant pathogen attacks are perceived through pathogen-issued compounds or plant-derived molecules that elicit defense reactions. Despite the large variety of elicitors, general schemes for cellular elicitor signaling leading to plant resistance can be drawn. In this article, we review early signaling events that happen after elicitor perception, including reversible protein phosphorylations, changes in the activities of plasma membrane proteins, variations in free calcium concentrations in cytosol and nucleus, and production of nitric oxide and active oxygen species. These events occur within the first minutes to a few hours after elicitor perception. One specific elicitor transduction pathway can use a combination or a partial combination of such events which can differ in kinetics and intensity depending on the stimulus. The links between the signaling events allow amplification of the signal transduction and ensure specificity to get appropriate plant defense reactions. This review first describes the early events induced by cryptogein, an elicitor of tobacco defense reactions, in order to give a general scheme for signal transduction that will be use as a thread to review signaling events monitored in different elicitor or plant models.

Nitric oxide (NO) has recently emerged as an important cellular mediator in plant defense responses. However, elucidation of the biochemical mechanisms by which NO participates in this signaling pathway is still in its infancy. We previously demonstrated that cryptogein, an elicitor of tobacco defense responses, triggers a NO burst within minutes in epidermal sections from tobacco leaves (Nicotiana tabacum cv Xanthi). Here, we investigate the signaling events that mediate NO production, and analyze NO signaling activities in the cryptogein transduction pathway. Using flow cytometry and spectrofluorometry, we observed that cryptogein-induced NO production in tobacco cell suspensions is sensitive to nitric oxide synthase inhibitors and may be catalyzed by variant P, a recently identified pathogen-inducible plant nitric oxide synthase. NO Moreover, NO appears to be involved in the pathway(s) leading to the accumulation of transcripts encoding the heat shock protein TLHS-1, the ethyleneforming enzyme cEFE-26, and cell death. In contrast, NO does not act upstream of the elicitor-induced activation of mitogenactivated protein kinase, the opening of anion channels, nor expression of GST, LOX-1, PAL, and PR-3 genes. Collectively, our data indicate that NO is intimately involved in the signal transduction processes leading to cryptogein-induced defense responses.Plants are frequently challenged by potential pathogens and have therefore evolved inducible defense mechanisms to survive in their environment. The activation of plant defense responses is initiated through the recognition of microorganism-derived molecules called elicitors, which trigger rapid defense responses via complex signal transduction pathways (Scheel, 1998). Plant defense responses classically include the production of active oxygen species (AOS), reinforcement of cell walls, and enhanced expression of a large number of defense-related genes, including those encoding cell wall proteins, enzymes involved in the phenylpropanoid biosynthetic pathway, and pathogenesis-related (PR) proteins (Fritig et al., 1998). Plants resisting pathogen attack sometimes develop a hypersensitive response (HR) in which rapid, localized cell death is associated with the restriction of invaders to the infection site (Lam et al., 2001). The HR shares some features of the apoptotic cell death process in animals, and it may likewise represent a type of programmed cell death (PCD; Lam et al., 2001). Moreover, plants usually develop a long-lasting resistance to diverse pathogens via systemic acquired resistance (SAR) or the less well understood induced systemic resistance (ISR; Pieterse et al., 1998).Cryptogein is a basic 10-kD proteinaceous elicitor secreted by the hemibiotrophic oomycete Phytophthora cryptogea (Ricci, 1997). The application of nanomolar concentrations of cryptogein to tobacco plants triggers expression of defense-related genes, induces an HR-like response, and inaugurates the protection of plants against invasion by a broad spectrum of microorganisms including...

SUMMARYThe three closely related Arabidopsis basic leucine zipper (bZIP) transcription factors TGA2, TGA5 and TGA6 are required for the establishment of the salicylic acid (SA)-dependent plant defense response systemic acquired resistance, which is effective against biotrophic pathogens. Here we show that the same transcription factors are essential for the activation of jasmonic acid (JA)-and ethylene (ET)-dependent defense mechanisms that counteract necrotrophic pathogens: the tga256 triple mutant is impaired in JA/ET-induced PDF1.2 and b-CHI expression, which correlates with a higher susceptibility against the necrotroph Botrytis cinerea. JA/ET induction of the trans-activators ERF1 and ORA59, which act upstream of PDF1.2, was slightly increased (ERF1) or unaffected (ORA59). PDF1.2 expression can be restored in the tga256 mutant by increased expression of ORA59, as observed in the tga256 jin1 quadruple mutant, which lacks the transcription factor JIN1/AtMYC2 that functions as a negative regulator of the JA/ET-dependent anti-fungal defense program. Whereas JA/ ET-induced PDF1.2 expression is strongly suppressed by SA in wild-type plants, no negative effect of SA on PDF1.2 expression was observed in the tga256 jin1 quadruple mutant. These results imply that the antagonistic effects of TGA factors and JIN1/AtMYC2 on the JA/ET pathway are necessary to evoke the SA-mediated suppression of JA/ET-induced defense responses.

The function of nitric oxide (NO), a gaseous free radical emitted by many plants, is incompletely understood. In the present study the hypothesis that NO generation, like that of the reactive oxygen species, occurs as a general response to different environmental cues was tested. Leaf peels and mesophyll cell suspensions of Nicotiana tabacum cv. Xanthi were loaded with the NO-specific fluorophore, diaminofluorescein, and subjected to an abiotic stressor. Light stress and mechanical injury had no apparent effect on NO production. In contrast, high temperatures, hyperosmotic stress, salinity and epi-illumination in a microscope all led to rapid surges in NO-induced fluorescence. The fluorescence originated from cells of the palisade mesophyll and across all epidermal cell types, including guard cells, subsidiary cells, and long and short trichomes. Fluorescence was evident first in the plastids, then in the nucleus and finally throughout the cytosol. Nicotiana plumbaginifolia cell suspensions expressing the calcium reporter aequorin provided evidence that, under hyperosmotic stress, NO participates in the elevation of free Ca 2+ + + + in the cytoplasm. The physiological significance of NO production in response to abiotic stressors is discussed.