At high concentrations, free radicals and radical-derived, nonradical reactive species are hazardous for living organisms and damage all major cellular constituents. At moderate concentrations, how...

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Free Radicals in the Physiological Control of Cell Function

▪ Abstract The transcription factor NF-κB, more than a decade after its discovery, remains an exciting and active area of study. The involvement of NF-κB in the expression of numerous cytokines and adhesion molecules has supported its role as an evolutionarily conserved coordinating element in the organism's response to situations of infection, stress, and injury. Recently, significant advances have been made in elucidating the details of the pathways through which signals are transmitted to the NF-κB:IκB complex in the cytosol. The field now awaits the discovery and characterization of the kinase responsible for the inducible phosphorylation of IκB proteins. Another exciting development has been the demonstration that in certain situations NF-κB acts as an anti-apoptotic protein; therefore, elucidation of the mechanism by which NF-κB protects against cell death is an important goal. Finally, the generation of knockouts of members of the NF-κB/IκB family has allowed the study of the roles of these protein...

NF-kappa B and Rel proteins: evolutionarily conserved mediators of immune responses

Phenylpropanoid compounds encompass a wide range of structural classes and biological functions. Limiting discussion to stress-induced phenylpropanoids eliminates few of the structural classes, because many compounds thst are constitutive in one plant species or tissue can be induced by various stresses in another species or in another tissue of the same plant (Beggs et al., 1987; Christie et al., 1994).

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Stress-Induced Phenylpropanoid Metabolism.

Plants cannot move to escape environmental challenges. Biotic stresses result from a battery of potential pathogens: fungi, bacteria, nematodes and insects intercept the photosynthate produced by plants, and viruses use replication machinery at the host's expense. Plants, in turn, have evolved sophisticated mechanisms to perceive such attacks, and to translate that perception into an adaptive response. Here, we review the current knowledge of recognition-dependent disease resistance in plants. We include a few crucial concepts to compare and contrast plant innate immunity with that more commonly associated with animals. There are appreciable differences, but also surprising parallels.

Plant pathogens and integrated defence responses to infection.

It has been suggested that effective defense against biotrophic pathogens is largely due to programmed cell death in the host, and to associated activation of defense responses regulated by the salicylic acid-dependent pathway. In contrast, necrotrophic pathogens benefit from host cell death, so they are not limited by cell death and salicylic acid-dependent defenses, but rather by a different set of defense responses activated by jasmonic acid and ethylene signaling. This review summarizes results from Arabidopsis-pathogen systems regarding the contributions of various defense responses to resistance to several biotrophic and necrotrophic pathogens. While the model above seems generally correct, there are exceptions and additional complexities.

Contrasting Mechanisms of Defense Against Biotrophic and Necrotrophic Pathogens

It has been proposed that salicylic acid acts as an endogenous signal responsible for inducing systemic acquired resistance in plants. The contribution of salicylic acid to systemic acquired resistance was investigated in transgenic tobacco plants harboring a bacterial gene encoding salicylate hydroxylase, which converts salicylic acid to catechol. Transgenic plants that express salicylate hydroxylase accumulated little or no salicylic acid and were defective in their ability to induce acquired resistance against tobacco mosaic virus. Thus, salicylic acid is essential for the development of systemic acquired resistance in tobacco.

http://science.sciencemag.org/content/sci/261/5122/754.full.pdf

Requirement of Salicylic Acid for the Induction of Systemic Acquired Resistance

Transgenic tobacco and Arabidopsis thaliana expressing the bacterial enzyme salicylate hydroxylase cannot accumulate salicylic acid (SA). This defect not only makes the plants unable to induce systemic acquired resistance, but also leads to increased susceptibility to viral, fungal, and bacterial pathogens. The enhanced susceptibility extends even to host-pathogen combinations that would normally result in genetic resistance. Therefore, SA accumulation is essential for expression of multiple modes of plant disease resistance.

https://science.sciencemag.org/content/sci/266/5188/1247.full.pdf

A Central Role of Salicylic Acid in Plant Disease Resistance

In a variety of plant species, the development of necrotic lesions in response to pathogen infection leads to induction of generalized disease resistance in uninfected tissues. A well-studied example of this "immunity" reaction is systemic acquired resistance (SAR) in tobacco. SAR is characterized by the development of a disease-resistant state in plants that have reacted hypersensitively to previous infection by tobacco mosaic virus. Here, we show that the onset of SAR correlates with the coordinate induction of nine classes of mRNAs. Salicylic acid, a candidate for the endogenous signal that activates the resistant state, induces expression of the same "SAR genes." A novel synthetic immunization compound, methyl-2,6-dichloroisonicotinic acid, also induces both resistance and SAR gene expression. These observations are consistent with the hypothesis that induced resistance results at least partially from coordinate expression of these SAR genes. A model is presented that ties pathogen-induced necrosis to the biosynthesis of salicylic acid and the induction of SAR.

Coordinate Gene Activity in Response to Agents That Induce Systemic Acquired Resistance.

Acquired resistance is an important component of the complex disease resistance mechanism in plants, which can result from either pathogen infection or treatment with synthetic, resistance-inducing compounds In this study, Arabidopsis, a tractable genetic system, is shown to develop resistance to a bacterial and a fungal pathogen following 2,6-dichloroisonicotinic acid (INA) treatment Three proteins that accumulated to high levels in the apoplast in response to INA treatment were purified and characterized Expression of the genes corresponding to these proteins was induced by INA, pathogen infection, and salicylic acid, the latter being a putative endogenous signal for acquired resistance Arabidopsis should serve as a genetic model for studies of this type of immune response in plants

Acquired resistance in Arabidopsis.

In the spectrum of plant-microbe interactions disease is a rare outcome. In many interactions complex, integrated defense mechanisms prevent infection and disease. These defensive systems include preformed physical and chemical barriers as well as inducible defenses such as the strengthening of cell walls or synthesis of antimicrobial compounds (i.e., phytoalexins) and proteins.1,2 In certain cases plants react to pathogen attack by developing long-lasting, broad-spectrum systemic resistance to later attacks by pathogens. This phenomenon, termed systemic acquired resistance (SAR), has been observed in many species and may be ubiquitous among higher plants. In the last five years progress has been made toward understanding the molecular basis of SAR. In this review we first provide a brief history of SAR research, then describe our present knowledge of the manifestation and induction of SAR. We discuss recent findings that indicate a central role for the SAR pathway in plant health and finally present our current working model of SAR induction.

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Scott Uknes

Papers

Requirement of Salicylic Acid for the Induction of Systemic Acquired Resistance

A Central Role of Salicylic Acid in Plant Disease Resistance

Coordinate Gene Activity in Response to Agents That Induce Systemic Acquired Resistance.

Acquired resistance in Arabidopsis.

Systemic Acquired Resistance