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Auxin
Signaling Pathway

AvrRpt2

Cui et al., 2013 and Chen et al., 2007 showed that AvrRpt2 is a type III secretion effector from Pseudomonas syringae pv. tomato DC3000 to promote auxin signaling. AvrRpt2 alters auxin signaling through targeted proteasomal degradation of Aux/IAA proteins to increase pathogen growth.

PSE1

PSE1 is a penetration specific effector secreted from the oomycete Phytophthora parasitica, Evangelisti et al., 2013 showed that targets auxin transport through enhanced activation of PIN transcription and sub-cellular localization. PSE1 increases auxin content at sites of infection and acts in suppressing SA-mediated defense responses to increase pathogen growth.

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Biosynthesis Pathway

AUX signaling pathway: AUX is perceived by auxin receptors that are part of a family of F-box proteins consisting of TIR1 and AFB proteins, all of which were a part of an E3-ligaes SCF complex.  The auxin binding to TIR1/AFB proteins increases the affinity of the SCF complex for the Aux/IAA transcriptional repressors leading to their degradation by 26S proteasome.  Degradation of the Aux/IAA transcriptional repressors results in the release of the transcriptional activators ARF, which are typically blocked by Aux/IAA proteins under conditions of low auxin levels. Release of ARF results in activation of AUX-dependent genes such as the auxin efflux carrier protein family PIN to create AUX gradients throughout the plant. Arrows indicate positive interaction; blunt-end indicates negative interaction (inhibition).

AUX biosynthesis pathway: AUX synthesis starts with synthesis of the most common form of auxin, indole-3-acetic acid or IAA. IAA can be synthesized via a tryptophan dependent and independent pathways. The tryptophan independent pathway involves converting IGP, indole-3-glycerol phosphate, to IAA or converting IGP to indole to form IAA.  IAA synthesis in plants is typically formed from the amino acid tryptophan, through one of four dependent pathways.  Arrows indicate positive interaction; blunt-end indicates negative interaction (inhibition).

There are no current examples of pathogens targeting this pathway.

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© 2016 Alexandra Shigenaga and Dr. Cris Argueso

Colorado State University, Fort Collins, CO 80523

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