Signaling Pathway
Biosynthesis Pathway
COR
Coronatine, COR, is a phytotoxin produced by many Pseudomonas syringae pathovars. Brooks et al., 2005 showed how COR assists P. syringae pathovars over-comes SA defenses, while Katsir et al., 2008 first showed that COR is a jasmonic acid-isoleucine structural mimic and acts as a competitor with jasmonic acid for binding to the COI1 receptor. When COR binds to the COI1 receptor this initiates JAZ protein degradation, causing an up regulation of jasmonic acid signaling while repressing the salicylic acid pathway. Studies suggest that this strategy is used as a means to regulate stomatal immunity and increase pathogen growth. Other studies including Zheng et al., 2012 focus on COR in relation to P. syringae and Uppalapati et al., 2007 focus on COR in relation to Pst DC3000.
HopX1
Gimenez-Ibanez et al., 2014 showed that HopX1 is a Pseudomonas syringae effector that acts are a cysteine protease, commonly found in many P. syringae pathovars that do not produce coronation. HopX1 targets JAZ proteins for degradation through it's protease activity, resulting in promoting jasmonic acid signaling and promoting pathogen virulence.
HopZ1
Jiang et al., 2013 showed that HopZ1 is a Pseudomonas syringae effector that has acetyltransferase activity and can interfere with the ZIM domain of JAZ proteins. This interference leads to acetylation and proteasome degradation of the JAZ proteins, resulting in jasmonic acid signaling being activated to promote pathogen virulence.
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FoxLox
Brodhun et al., 2013 showed that Fusarium oxysporum can produce bioactive derivatives of jasmonic acid through an iron 13S-LIPOXYGENASE (FoxLox), similar to LOX enzymes used by plants to synthesis jasmonic acid. This allows F. oxysporum to increase the jasmonic acid synthesis to inhibit the salicylic acid pathway and salicylic acid-mediated defense responses.
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JA signaling pathway: Perception of JA is controlled by the JA receptor COI1, an E3 ligase SCF F-box protein, and transcriptional repressor JAZ proteins. JAZ proteins associate with the adaptor proteins NINJA and transcriptional repressor TPL, in the absence of JA. After JAZ associated with TPL through an EAR domain, there is an initiation of chromatin modification through the recruitment of histone modifying enzymes HDA6, HDA9, and HMT to repress JA-mediated responses. The JAZ-NINJA-TPL complex associated with MYC and ERF transcription factors, resulting in activation of two sets of JA-regulated genes. MYC transcription factors initiate the transcription activity of VSP2, which the other branch regulated by ERF transcription factors regulates expression of PDF1.2 to activate JA-mediated defense responses. In addition, JAZ proteins can directly bind to the a subunit of the MED25 complex to block MYC3 from binding MED25 to block MYC3 activated JA defense responses. Arrows indicate positive interaction; blunt-end indicates negative interaction (inhibition).
JA biosynthetic pathway: alpha-linolenic acid is first released from chloroplast membranes and then oxygenated by LOX, AOS, and AOC enzymes to OPDA, 12-oxo-phytodienoic acid. Once oxygenated OPDA is converted to JA by OPR3 and β-oxygenation; from here JA can be converted to various JA derivatives. JA can be converted to the endogenously biologically active JA-Ile, (+)-7-iso-jasmonoyl-l-isoleucine, by the enzyme JAR1. JA can be converted into a volatile form of MeJA, methyl jasmonate, via methylation by the enzyme JMT. Arrows indicate positive interaction; blunt-end indicates negative interaction (inhibition).
