biostudies-literatureUnknown11(6)Mitra AThe quorum sensing molecule Autoinducer-2 (AI-2) is generated as a byproduct of activated methyl cycle by the action of LuxS in Escherichia coli. AI-2 is synthesized, released and later internalized in a cell-density dependent manner. Here, by mutational analysis of the genes, uvrY and csrA, we describe a regulatory circuit of accumulation and uptake of AI-2. We constructed a single-copy chromosomal luxS-lacZ fusion in a luxS + merodiploid strain and evaluated its relative expression in uvrY and csrA mutants. At the entry of stationary phase, the expression of the fusion and AI-2 accumulation was positively regulated by uvrY and negatively regulated by csrA respectively. A deletion of csrA altered message stability of the luxS transcript and CsrA protein exhibited weak binding to 5' luxS rPloS onee0157532https://www.ebi.ac.uk/biostudies/studies/S-EPMC4928848biostudies-literatureIntegration of AI-2 Based Cell-Cell Signaling with Metabolic Cues in Escherichia coli.PMC4928848Patel IRColeman AMitra AMukhopadhyay SHerren CDfalseIntegration of AI-2 Based Cell-Cell Signaling with Metabolic Cues in Escherichia coli.The quorum sensing molecule Autoinducer-2 (AI-2) is generated as a byproduct of activated methyl cycle by the action of LuxS in Escherichia coli. AI-2 is synthesized, released and later internalized in a cell-density dependent manner. Here, by mutational analysis of the genes, uvrY and csrA, we describe a regulatory circuit of accumulation and uptake of AI-2. We constructed a single-copy chromosomal luxS-lacZ fusion in a luxS + merodiploid strain and evaluated its relative expression in uvrY and csrA mutants. At the entry of stationary phase, the expression of the fusion and AI-2 accumulation was positively regulated by uvrY and negatively regulated by csrA respectively. A deletion of csrA altered message stability of the luxS transcript and CsrA protein exhibited weak binding to 5' luxS r2016-01-01T00:00:00Z20162026-04-08T16:01:30.255Z2026-04-08T05:56:26.72ZS-EPMC49288482736250710.1371/journal.pone.0157532