Abstract
To accomplish successful infection, pathogens deploy complex strategies to interfere with host defense systems and subvert host physiology to favor pathogen survival and multiplication. Modulation of plant auxin physiology and signaling is emerging as a common virulence strategy for phytobacteria to cause diseases. However, the underlying mechanisms remain largely elusive. We have previously shown that the Pseudomonas syringae type III effector AvrRpt2 alters Arabidopsis (Arabidopsis thaliana) auxin physiology. Here, we report that AvrRpt2 promotes auxin response by stimulating the turnover of auxin/indole acetic acid (Aux/IAA) proteins, the key negative regulators in auxin signaling. AvrRpt2 acts additively with auxin to stimulate Aux/IAA turnover, suggesting distinct, yet proteasome-dependent, mechanisms operated by AvrRpt2 and auxin to control Aux/IAA stability. Cysteine protease activity is required for AvrRpt2-stimulated auxin signaling and Aux/IAA degradation. Importantly, transgenic plants expressing the dominant axr2-1 mutation recalcitrant to AvrRpt2-mediated degradation ameliorated the virulence functions of AvrRpt2 but did not alter the avirulent function mediated by the corresponding RPS2 resistance protein. Thus, promoting auxin response via modulating the stability of the key transcription repressors Aux/IAA is a mechanism used by the bacterial type III effector AvrRpt2 to promote pathogenicity.
Highlights
To accomplish successful infection, pathogens deploy complex strategies to interfere with host defense systems and subvert host physiology to favor pathogen survival and multiplication
Consistent with auxin’s role in plant disease resistance, we have found that the P. syringae effector AvrRpt2 augments host auxin biosynthesis and signaling and alters auxin physiology (Chen et al, 2007)
Recent studies demonstrated that auxin binds TIR1 and stabilizes the interaction between TIR1 and its auxin/indole acetic acid (Aux/IAA) substrates
Summary
Pathogens deploy complex strategies to interfere with host defense systems and subvert host physiology to favor pathogen survival and multiplication. The type III secretion system mediates the delivery of a plethora of effector proteins into host cells, where they sabotage host immune responses and physiology to favor pathogen survival and multiplication in susceptible plants and trigger defense responses in resistant plants (Mudgett, 2005; Göhre and Robatzek, 2008; Büttner and He, 2009; Block and Alfano, 2011; Feng and Zhou, 2012; Lindeberg et al, 2012). Many type III effectors are able to interfere with or suppress host immunity by directly hijacking key components in PTI signaling (Mudgett, 2005; Göhre and Robatzek, 2008; Büttner and He, 2009; Block and Alfano, 2011; Feng and Zhou, 2012; Lindeberg et al, 2012) It is much less understood how these effectors modulate host physiology to favor infection. Auxin is associated with disease susceptibility, and the suppression of auxin signaling appears to constitute a part of plant defense mechanisms
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