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

Abstract

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 <i>Hydra</i> is able to modify bacterial quorum-sensing signals. We identified a eukaryotic mechanism that enables <i>Hydra</i> to specifically modify long-chain 3-oxo-homoserine lactones into their 3-hydroxy-HSL counterparts. Expression data revealed that <i>Hydra</i>'s main bacterial colonizer, <i>Curvibacter</i> sp., responds differentially to <i>N</i>-(3-hydroxydodecanoyl)-l-homoserine lactone (3OHC12-HSL) and <i>N</i>-(3-oxododecanoyl)-l-homoserine lactone (3OC12-HSL). Investigating the impacts of the different <i>N</i>-acyl-HSLs on host colonization elucidated that 3OHC12-HSL allows and 3OC12-HSL represses host colonization of <i>Curvibacter</i> 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.