Signaling Pathway
XopJ
Ustun et al., 2013 showed that XopJ is an effector from Xanthomonas euvesicatoria, a biographic pathogen, that interferes with NPR1 activity. XopJ interferes with NPR1 activity through interacting with RPT6, important protease of proteasome pathway that regulates NPR1 turnover. Interference with NPR1 turnover results in inhibiting SA signaling.
SyrA
Schellenberg et al., 2010 showed that SyrA, syringolin A, is a toxin secreted by Pseudomonas syringae pv syringe that acts as a proteasome inhibitor by inhibiting NPR1 turnover resulting in suppression of SA signaling.
HaRxL44
HaRxL44 is one of many HaRxLs, ExLR effectors from the pathogen Hyaloperonospora arabidopsidis. HaRxL effectors are target components of the Mediator complex (MED), a protein complex that is important for specific transcription factors and transcriptional machinery of various eukaryotes. This is important because the MED complex plays a key role in SA-mediated defense regulation. Caillaud et al., 2013 shows that HaRxL44 decreases PR-1 expression by interacting with the MED complex and activating it's degradation, decreasing overall SA signaling and SA-mediated responses.
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Biosynthesis Pathway
Cmu1
Djamei et al., 2011 showed that Cmu1 is an effector from the Ustilago maydis that interferes with the SA biosynthetic pathway. Cmu1 acts as a chorismate mutase enzyme that converts chorismate to prephenate, lowering chorismate levels for conversion to SA by ICS, and not allowing SA to accumulate in response to infection.
COR
Coronatine, COR, is a phytotoxin secreted by several Pseudomonas syringae pathovars. COR is a JA-Ile, jasmonic isoleucine, mimic and de Torres-Zabala et al., 2009 showed that COR can decrease SA biosynthesis through inhibiting ICS1 expression.
COR (BSMT)
Zheng et al., 2012 has shown that COR acts on the SA pathway through three NAC transcription factors, which are targets of a JA-regulated transcription factor called MYC2. MYC2 leads to imitation of the three NAC transcription factors that act downstream of ICS1 and up-regulate expression of the methyltransferase BSMT1, resulting in overall decreased levels of biologically active SA derivatives.
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SA Signaling Pathway: NPR1 is known as the master regulator of SA-mediated defense responses. In addition to NPR1, the NPR1 paralogues NPR3 and NPR4 bind SA and function as SA receptors. Turnover of nuclear NPR1 is conducted by the 26S proteasome pathway consisting of the SCFNPR3/NPR4 complex, which fine-tunes NPR1 availability for SA-dependent gene expression. NIMIN proteins interact with NPR1 and mostly act as negative regulators of NPR1. In the nucleus, NPR1 can interact with TGA factors. TGA factors can bind to PR-1 promoter region after interacting with NPR1 to repress gene expression. The Meditator complex, is a protein complex that acts as a bridge between transcription factors and transcriptional machinery, playing a key role in transcription regulation. The Mediator complex plays an integral role in SA-mediated gene expression, and therefore contributes to expression of the SA-mediated defense gene PR-1. Arrows indicate positive interaction; blunt-end indicates negative interaction (inhibition).
SA Biosynthesis Pathway: SA is synthesized in the chloroplast from the primary metabolite chorismate by two major pathways. One pathway involves PAL and the other involves a two-step process by ICS and IPL. PAL converts phenylalanine to cinnamic acid before converting cinnamic acid into one of two SA precursors, O-coumaric acid or benzoate intermediates. In the two-step pathway, ICS converts chorismate to isochorismate and IPL converts isochorismate into SA. After synthesis in the chloroplast, SA can then be converted to various derivatives such as SAG, biologically inactive SA beta-glucoside, by SAGT or MeSA, inactive volatile form, by BSMT/SAMT in the cytosol. Arrows indicate positive interaction; blunt-end indicates negative interaction (inhibition).
