Abstract
Activation of salicylic acid (SA) biosynthesis in association with changes in redox homeostasis occurs in plants exposed to diverse biotic and abiotic stresses such as pathogens infection, excess of UV radiation, or increased levels of ozone (O3). Under these conditions, reactive oxygen species (ROS) and SA are the crucial signals for triggering defense-related processes that are genetically controlled, e.g. programmed cell death (PCD) and the expression of genes that cause defense against stress. Increasing evidence in the yesteryears supports the idea that SA interplays with ROS in the genetic-controlled defense reactions. In this chapter we discuss this evidence, particularly focusing on the expression of stress defense genes. In the first section we are giving an overview about how the changes in SA levels and redox homeostasis occur in the establishment of the defense reaction against stressful conditions. In the second section we will review the information obtained from genetic and biochemical approaches about signaling proteins and promoter DNA elements, involved in the activation of defense genes by SA. Redox controlled transcriptional co-regulators, transcription factors and promoter DNA elements have been shown to mediate SA induced activation of these genes. In the third section we are going to analyze available transcriptome data obtained from Arabidopsis plants, either treated with SA or analogs or subjected to stress conditions. We have classified the up-regulated genes according to their known or putative functions. Interestingly, we found genes coding for proteins with antioxidant and detoxifying functions, together with other defense-related functions. Taking together, these evidences suggest that SA plays a role in controlling the cellular redox balance at the onset of the defense response.
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Holuigue, L., Salinas, P., Blanco, F., GarretÓn, V. (2007). Salicylic Acid and Reactive Oxygen Species in the Activation of Stress Defense Genes. In: Hayat, S., Ahmad, A. (eds) Salicylic Acid: A Plant Hormone. Springer, Dordrecht. https://doi.org/10.1007/1-4020-5184-0_8
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