Salicylic acid (SA) or 2-hydroxybenoic acid is a phenolic plant hormone that plays an essential role in plant defense against biotrophic and semi-biotrophic pathogens. In Arabidopsis, SA is synthesized from chorismate in the chloroplast through the ICS1 (isochorismate synthase I) pathway during pathogen infection. The transcription co-activator NPR1 (Non-Expresser of Pathogenesis-Related Gene 1), as the master regulator of SA signaling, interacts with transcription factors to induce the expression of anti-microbial PR (Pathogenesis-Related) genes. To establish successful infections, plant bacterial, oomycete, fungal, and viral pathogens have evolved at least three major strategies to disrupt SA-mediated defense. The first strategy is to reduce SA accumulation directly by converting SA into its inactive derivatives. The second strategy is to interrupt SA biosynthesis by targeting the ICS1 pathway. In the third major strategy, plant pathogens deploy different mechanisms to interfere with SA downstream signaling. The wide array of strategies deployed by plant pathogens highlights the crucial role of disruption of SA-mediated plant defense in plant pathogenesis. A deeper understanding of this topic will greatly expand our knowledge of how plant pathogens cause diseases and consequently pave the way for the development of more effective ways to control these diseases.
Keywords: NPR1; PR proteins; VIGS; effectors; salicylic acid; toxin.
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