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Title: The bacterial quorum sensing signal DSF hijacks Arabidopsis thaliana sterol biosynthesis to suppress plant innate immunity
Authors: Tran, T.M.
Ma, Z.
Triebl, A. 
Nath, S.
Cheng, Y.
Gong, B.-Q.
Han, X.
Wang, J.
Li, J.-F.
Wenk, M.R. 
Torta, F. 
Mayor, S.
Yang, L.
Miao, Y.
Issue Date: 2020
Publisher: Rockefeller University Press
Citation: Tran, T.M., Ma, Z., Triebl, A., Nath, S., Cheng, Y., Gong, B.-Q., Han, X., Wang, J., Li, J.-F., Wenk, M.R., Torta, F., Mayor, S., Yang, L., Miao, Y. (2020). The bacterial quorum sensing signal DSF hijacks Arabidopsis thaliana sterol biosynthesis to suppress plant innate immunity. Life Science Alliance 3 (10) : e202000720. ScholarBank@NUS Repository.
Rights: Attribution 4.0 International
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. © This article is available under a Creative Commons License (Attribution 4.0 International, as described at
Source Title: Life Science Alliance
ISSN: 25751077
DOI: 10.26508/LSA.202000720
Rights: Attribution 4.0 International
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