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Host modification of a bacterial quorum-sensing signal induces a phenotypic switch in bacterial symbionts

MPG-Autoren
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Künzel,  Sven
Department Evolutionary Genetics, Max Planck Institute for Evolutionary Biology, Max Planck Society;

Externe Ressourcen

http://www.pnas.org/content/114/40/E8488
(Verlagsversion)

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Zitation

Pietschke, C., Treitz, C., Forêt, S., Schultze, A., Künzel, S., Tholey, A., et al. (2017). Host modification of a bacterial quorum-sensing signal induces a phenotypic switch in bacterial symbionts. Proceedings of the National Academy of Sciences of the United States of America, 114(40), E8488-E8497. doi:10.1073/pnas.1706879114.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-002E-2DB7-1
Zusammenfassung
Bacterial communities colonize epithelial surfaces of most animals. Several factors, including the innate immune system, mucus composition, and diet, have been identified as determinants of host-associated bacterial communities. Here we show that the early branching metazoan Hydra is able to modify bacterial quorum-sensing signals. We identified a eukaryotic mechanism that enables Hydra to specifically modify long-chain 3-oxo-homoserine lactones into their 3-hydroxy-HSL counterparts. Expression data revealed that Hydra’s main bacterial colonizer, Curvibacter sp., responds differentially to N-(3-hydroxy-dodecanoyl)-L-homoserine lactone (3OHC12-HSL) and N-(3-oxodode-canoyl)-L-homoserine lactone (3OC12-HSL). Investigating the impacts of the different N-acyl-HSLs on host colonization elucidated that 3OHC12-HSL allows and 3OC12-HSL represses host colonization of Curvibacter sp. These results show that an animal manipulates bacterial quorum-sensing signals and that this modification leads to a phenotypic switch in the bacterial colonizers. This mechanism may enable the host to manipulate the gene expression and thereby the behavior of its bacterial colonizers. © 2017, National Academy of Sciences. All rights reserved.