The relationship between basal and induced resistance in Arabidopsis

Plants are constantly exposed to potentially pathogenic micro-organisms. They possess an extensive array of passive and active defense mechanisms, and only a small proportion of micro-organisms are capable of infecting the plant and causing disease. Plant resistance can be broadly defined as the plant's ability to suppress or retard the damaging activity of a pathogen. The most common type of resistance is nonhost resistance. This type of resistance protects the plant entirely from infection by most potential pathogens, and is manifested as an inability of the pathogen to cause disease upon contact with any individual of a particular plant species. In such an interaction, the pathogen is nonpathogenic

Salicylic Acid Biosynthesis and Metabolism

Salicylic acid (SA) has been shown to regulate various aspects of growth and development; it also serves as a critical signal for activating disease resistance in Arabidopsis thaliana and other plant species. This review surveys the mechanisms involved in the biosynthesis and metabolism of this critical plant hormone. While a complete biosynthetic route has yet to be established, stressed Arabidopsis appear to synthesize SA primarily via an isochorismate-utilizing pathway in the chloroplast. A distinct pathway utilizing phenylalanine as the substrate also may contribute to SA accumulation, although to a much lesser extent. Once synthesized, free SA levels can be regulated by a variety of chemical modifications. Many of these modifications inactivate SA; however, some confer novel properties that may aid in long distance SA transport or the activation of stress responses complementary to those induced by free SA. In addition, a number of factors that directly or indirectly regulate the expression of SA biosynthetic genes or that influence the rate of SA catabolism have been identified. An integrated model, encompassing current knowledge of SA metabolism in Arabidopsis, as well as the influence other plant hormones exert on SA metabolism, is presented