Abstract
It is now well established that bacterial populations utilize cell-to-cell signaling (quorum-sensing, QS) to control the production of public goods and other co-operative behaviours. Evolutionary theory predicts that both the cost of signal production and the response to signals should incur fitness costs for producing cells. Although costs imposed by the downstream consequences of QS have been shown, the cost of QS signal molecule (QSSM) production and its impact on fitness has not been examined. We measured the fitness cost to cells of synthesising QSSMs by quantifying metabolite levels in the presence of QSSM synthases. We found that: (i) bacteria making certain QSSMs have a growth defect that exerts an evolutionary cost, (ii) production of QSSMs negatively correlates with intracellular concentrations of QSSM precursors, (iii) the production of heterologous QSSMs negatively impacts the production of a native QSSM that shares common substrates, and (iv) supplementation with exogenously added metabolites partially rescued growth defects imposed by QSSM synthesis. These data identify the sources of the fitness costs incurred by QSSM producer cells, and indicate that there may be metabolic trade-offs associated with QS signaling that could exert selection on how signaling evolves.
Highlights
Communication systems are widespread in plants, animals and microorganisms
To test whether QS signal molecule (QSSM) synthesis is metabolically costly, the genes encoding QSSM synthases LasI and RhlI were expressed from the low copy number shuttle vector pME6032 in E. coli
Having hypothesized that QSSM synthesis would compromise cell fitness, the growth profiles of the strains were compared in both minimal (MMM; Fig. 1) and rich (LB; Supplementary Figs S4 and S5) media
Summary
Communication systems are widespread in plants, animals and microorganisms. For true communication (signaling) to evolve, signals must transfer information that benefits both the signaler and the receiver. LasI and RhlI were each introduced into a heterologous host, Escherichia coli, that does not naturally produce AHLs. We reasoned that it is important to determine whether there are fitness costs associated with QSSM production per se. A future challenge remains with respect to understanding the fitness burden of a complete QS system in its natural, adapted host In this context, it would be possible to consider the added cost of responding to the QSSM: this may in turn be integrated into a complex regulatory network or have pleiotropic effects unlinked to the response to signals. The donation of the acyl group from acyl-ACP to the amine of SAM results in the formation of the AHL and release of 5′-methylthioadenosine (MTA)[15,16,18] Both LasI and RhlI use SAM, but link it to a different fatty acid. Our findings demonstrate that the fitness cost of generating the QS signals required for co-ordinated social behaviour in bacteria can be substantial
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