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• W2928590920 abstract "The disruption of bacterial signaling (quorum quenching) has been proven to be an innovative approach to influence the behavior of bacteria. In particular, lactonase enzymes that are capable of hydrolyzing the N- acyl homoserine lactone (AHL) molecules used by numerous bacteria, were reported to inhibit biofilm formation, including those of freshwater microbial communities. However, insights and tools are currently lacking to characterize, understand and explain the effects of signal disruption on complex microbial communities. Here, we produced silica capsules containing an engineered lactonase that exhibits quorum quenching activity. Capsules were used to design a filtration cartridge to selectively degrade AHLs from a recirculating bioreactor. The growth of a complex microbial community in the bioreactor, in the presence or absence of lactonase, was monitored over a 3-week period. Dynamic population analysis revealed that signal disruption using a quorum quenching lactonase can effectively reduce biofilm formation in the recirculating bioreactor system and that biofilm inhibition is concomitant to drastic changes in the composition, diversity and abundance of soil bacterial communities within these biofilms. Effects of the quorum quenching lactonase on the suspension community also affected the microbial composition, suggesting that effects of signal disruption are not limited to biofilm populations. This unexpected finding is evidence for the importance of signaling in the competition between bacteria within communities. This study provides foundational tools and data for the investigation of the importance of AHL-based signaling in the context of complex microbial communities." @default.
• W2928590920 created "2019-04-11" @default.
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• W2928590920 date "2019-03-29" @default.
• W2928590920 modified "2023-10-05" @default.
• W2928590920 title "Signal Disruption Leads to Changes in Bacterial Community Population" @default.
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• W2928590920 doi "https://doi.org/10.3389/fmicb.2019.00611" @default.
• W2928590920 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6449428" @default.
• W2928590920 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/30984139" @default.
• W2928590920 hasPublicationYear "2019" @default.
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