Abstract

Quorum sensing (QS) is a recognized phenomenon that is crucial for regulating population-related behaviors in bacteria. However, the direct specific effect of QS molecules on host biology is largely understudied. In this work, we show that the QS molecule DSF (cis-11-methyl-dodecenoic acid) produced by Xanthomonas campestris pv. campestris can suppress pathogen-associated molecular pattern-triggered immunity (PTI) in Arabidopsis thaliana, mediated by flagellin-induced activation of flagellin receptor FLS2. The DSF-mediated attenuation of innate immunity results from the alteration of FLS2 nanoclusters and endocytic internalization of plasma membrane FLS2. DSF altered the lipid profile of Arabidopsis, with a particular increase in the phytosterol species, which impairs the general endocytosis pathway mediated by clathrin and FLS2 nano-clustering on the plasma membrane. The DSF effect on receptor dynamics and host immune responses could be entirely reversed by sterol removal. Together, our results highlighted the importance of sterol homeostasis to plasma membrane organization and demonstrate a novel mechanism by which pathogenic bacteria use their communicating molecule to manipulate pathogen-associated molecular pattern-triggered host immunity.

Highlights

  • Bacteria use quorum sensing (QS) to precisely coordinate population behaviors in response to various environmental cues

  • We asked whether diffusible signal factor (DSF), a recently discovered QS signal produced by diverse Gram-negative pathogens (Ryan et al, 2015), could dysregulate plant growth and pathogenassociated molecular pattern (PAMP)-triggered immunity (PTI) responses

  • The use of a non-DSF–producing bacterium here (Pst DC3000) was to differentiate the direct effect of DSF on plant immunity versus the effect of DSF through the activation of the bacterial type III secretion system and other traits regulated by QS in X. campestris pv. campestris (Xcc), which would otherwise be difficult to dissect as DSF-deficient or overproducing mutants are less virulent on plants (Torres et al, 2007; Gudesblat et al, 2009)

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Summary

Introduction

Bacteria use quorum sensing (QS) to precisely coordinate population behaviors in response to various environmental cues. QS signals are small molecules that contribute to bacterial virulence in bacterial–host interactions by either regulating bacterial type III secretion or priming host immune systems (Newman et al, 2004; Chatterjee et al, 2008; Brock et al, 2010). The contribution of QS signals to bacterial pathogenicity has been examined extensively, the direct effects of these small molecules on host biology remain under-explored. Plant pathogenic bacteria secrete small-molecule virulence factors to cross-talk with host and manipulate host immunity during infection. The detailed mechanisms of how QS molecules directly influence plant host development and pathology, especially the PAMPmediated host immunity, remains elusive

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