Pandemonium Breaks Out: Disruption of Salicylic Acid-Mediated Defense by Plant Pathogens

Abstract

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.

Genetic analysis of salicylic acid-mediated defenses responses and histopathology in the huanglongbing pathosystem

“…Downregulation of SA biosynthesis genes can be explained by two hypotheses: SA level in both stages evaluated in this work is high, thus the expression of ICS1 and PAL genes is low because SA synthesis is no more necessary or ICS1 is potentially targeted by CaL. to suppress SA-mediated plant immunity, as showed to other plant pathogens (Qi et al, 2018). For SA metabolism, BSMT1 (BENZOIC ACID/SALICYLIC ACID CARBOXYL METHYLTRANSFERASE1) -a SA metabolic enzyme gene -had significant level of induction in late stage of infection of both CLas and CLam (Figure 2).…”

“…However, MeSA seems not to be the only molecule essential to establish SAR (Attaran et al, 2009;Zheng et al, 2012;Maruri-López et al, 2019), and several candidate molecules have been suggested (Shah & Zeier, 2013). Moreover, some pathogens manipulate phytohormone pathways, converting SA to inactive derivatives as MeSA, to bypass defenses responses (Cui et al, 2005;Qi et al, 2018). In A. thaliana, Pseudomonas syringae prevents the SA accumulation by inducing the SA metabolic gene BSMT1 and repressing SA synthesis gene ICS1, similar to what was observed in late stages of CLam inoculated-citrus plants (Table 2).…”

“…SA-mediated defense seems not to be infallible because CaL. possibly have ways to overcome plant defense mechanism, as to direct lower SA accumulation by converting SA to inactive derivatives as MeSA, to interrupt SA biosynthesis by targeting specific pathways and to interfere with SA signaling (Qi et al 2018). Li et al (2017) showed that CLas may suppress plant defense by employing an active salicylate hydroxylase, thus halting SA accumulation and HR and allowing the pathogen to overcome the host defense.…”

Chloroplasts and Plant Immunity: Where Are the Fungal Effectors?

“…One pathway converts chorismate to isochorismate via isochorismate synthase (ICS1) in the chloroplast with subsequent conversion of isochorismate to SA in the cytosol [15]. A second pathway accounts for~10% of SA synthesis by converting isochorismate to SA via the phenylalanine ammonia-lyase pathway in the cytosol [3,4,8,15,16]. Phenylalanine is also synthesized in the chloroplast from chorismate [5].…”

The Arabidopsis Hypoxia Inducible AtR8 Long Non-Coding RNA also Contributes to Plant Defense and Root Elongation Coordinating with WRKY Genes under Low Levels of Salicylic Acid

“…In the absence of SA, oligomerized NPR1 proteins are retained in the cytoplasm, but SA-activated NPR1s are reduced together with cellular redox changes, monomerized, and translocated to the nucleus. Monomeric NPR1 does not exhibit DNA-binding activity as a TF; instead, it regulates target genes by interacting with a wide range of transcription activators, repressors, and cofactors that include members of the WRKY and bZIP transcription factor TGA families as well as NIM1-interacting proteins (NIMINs) [57,58]. NPR1 was proposed to regulate the transcription of PR genes together with the TGA family TF as a cofactor [59].…”