Global analysis of candidate genes important for fitness in a competitive biofilm using DNA-array-based transposon mapping

Junker, Lauren M.; Peters, Joseph E.

doi:10.1099/mic.0.28767-0

Cited by 33 publications

(31 citation statements)

References 70 publications

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“…The first three of these RRs were previously shown to be involved in biofilm formation in other bacteria (10,11,13,24,35). In particular, VF0454 encodes a protein with high sequence identity to the Vibrio cholerae exopolysaccharide regulator VpsR; a distinct study from our laboratory has also uncovered an important role for VF0454 in biofilm formation (3a).…”

Section: Discussionmentioning

confidence: 87%

RscS Functions Upstream of SypG To Control the syp Locus and Biofilm Formation in Vibrio fischeri

2008

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Two-component signal transduction systems, composed of sensor kinase (SK) and response regulator (RR) proteins, allow bacterial cells to adapt to changes such as environmental flux or the presence of a host. RscS is an SK required for Vibrio fischeri to initiate a symbiotic partnership with the Hawaiian squid Euprymna scolopes, likely due to its role in controlling the symbiosis polysaccharide (syp) genes and thus biofilm formation. To determine which RR(s) functions downstream of RscS, we performed epistasis experiments with a library of 35 RR mutants. We found that several RRs contributed to RscS-mediated biofilm formation in V. fischeri. However, only the syp-encoded symbiosis regulator SypG was required for both biofilm phenotypes and syp transcription induced by RscS. These data support the hypothesis that RscS functions upstream of SypG to induce biofilm formation. In addition, this work also revealed a role for the syp-encoded RR SypE in biofilm formation. To our knowledge, no other study has used a large-scale epistasis approach to elucidate twocomponent signaling pathways. Therefore, this work both contributes to our understanding of regulatory pathways important for symbiotic colonization by V. fischeri and establishes a paradigm for evaluating two-component pathways in the genomics era.

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Section: Discussionmentioning

confidence: 87%

RscS Functions Upstream of SypG To Control the syp Locus and Biofilm Formation in Vibrio fischeri

2008

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“…First, tynA mutants express the SOS response constitutively, which has been interpreted as indicating that the amine oxidase is responsible for removing an endogenously generated genotoxic compound (30). Second, feaB was identified in a screen for genes important for survival under planktonic (versus biofilm) growth conditions (20). This observation implies that a substrate for FeaB was present in the minimal growth medium used or can be generated endogenously.…”

Section: Discussionmentioning

confidence: 91%

Escherichia coli NsrR Regulates a Pathway for the Oxidation of 3-Nitrotyramine to 4-Hydroxy-3-Nitrophenylacetate

Rankin

Bodenmiller²,

Partridge

et al. 2008

J Bacteriol

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Chromatin immunoprecipitation and microarray (ChIP-chip) analysis showed that the nitric oxide (NO)-sensitive repressor NsrR from Escherichia coli binds in vivo to the promoters of the tynA and feaB genes. These genes encode the first two enzymes of a pathway that is required for the catabolism of phenylethylamine (PEA) and its hydroxylated derivatives tyramine and dopamine. Deletion of nsrR caused small increases in the activities of the tynA and feaB promoters in cultures grown on PEA. Overexpression of nsrR severely retarded growth on PEA and caused a marked repression of the tynA and feaB promoters. Both the growth defect and the promoter repression were reversed in the presence of a source of NO. These results are consistent with NsrR mediating repression of the tynA and feaB genes by binding (in an NO-sensitive fashion) to the sites identified by ChIP-chip. E. coli was shown to use 3-nitrotyramine as a nitrogen source for growth, conditions which partially induce the tynA and feaB promoters. Mutation of tynA (but not feaB) prevented growth on 3-nitrotyramine. Growth yields, mutant phenotypes, and analyses of culture supernatants suggested that 3-nitrotyramine is oxidized to 4-hydroxy-3-nitrophenylacetate, with growth occurring at the expense of the amino group of 3-nitrotyramine. Accordingly, enzyme assays showed that 3-nitrotyramine and its oxidation product (4-hydroxy-3-nitrophenylacetaldehyde) could be oxidized by the enzymes encoded by tynA and feaB, respectively. The results suggest that an additional physiological role of the PEA catabolic pathway is to metabolize nitroaromatic compounds that may accumulate in cells exposed to NO.

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“…Bacterial biofilms are ubiquitous, and they have been extensively investigated under a variety of conditions. While there is increasing interest in bacterial biofilm formation in the gastrointestinal (GI) tract (30,40), the genetic basis of EHEC biofilm formation is not well studied, whereas there are four singletime-point microarray studies of E. coli K-12 biofilm formation (5,32,51,59) and one temporal study (11).…”

Section: Discussionmentioning

confidence: 99%

EnterohemorrhagicEscherichia coliBiofilms Are Inhibited by 7-Hydroxyindole and Stimulated by Isatin

Lee

Bansal²,

Jayaraman³

et al. 2007

Appl Environ Microbiol

177

188

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Since indole is present at up to 500 M in the stationary phase and is an interspecies biofilm signal (J. Lee, A. Jayaraman, and T. K. Wood, BMC Microbiol. 7:42, 2007), we investigated hydroxyindoles as biofilm signals and found them also to be nontoxic interspecies biofilm signals for enterohemorrhagic Escherichia coli O157:H7 (EHEC), E. coli K-12, and Pseudomonas aeruginosa. The genetic basis of EHEC biofilm formation was also explored, and notably, virulence genes in biofilm cells were repressed compared to those in planktonic cells. In Luria-Bertani medium (LB) on polystyrene with quiescent conditions, 7-hydroxyindole decreased EHEC biofilm formation 27-fold and decreased K-12 biofilm formation 8-fold without affecting the growth of planktonic cells. 5-Hydroxyindole also decreased biofilm formation 11-fold for EHEC and 6-fold for K-12. In contrast, isatin (indole-2,3-dione) increased biofilm formation fourfold for EHEC, while it had no effect for K-12. When continuous-flow chambers were used, confocal microscopy revealed that EHEC biofilm formation was reduced 6-fold by indole and 10-fold by 7-hydroxyindole in LB. Whole-transcriptome analysis revealed that isatin represses indole synthesis by repressing tnaABC 7-to 37-fold in EHEC, and extracellular indole levels were found to be 20-fold lower. Furthermore, isatin repressed the AI-2 transporters lsrABCDFGKR, while significantly inducing the flagellar genes flgABCDEFGHIJK and fliAEFGILMNOPQ (which led to a 50% increase in motility). 7-Hydroxyindole induces the biofilm inhibitor/stress regulator ycfR and represses cysADIJPU/fliC (which led to a 50% reduction in motility) and purBCDEFHKLMNRT. Isogenic mutants showed that 7-hydroxyindole inhibits E. coli biofilm through cysteine metabolism. 7-Hydroxyindole (500 M) also stimulates P. aeruginosa PAO1 biofilm formation twofold; therefore, hydroxyindoles are interspecies bacterial signals, and 7-hydroxyindole is a potent EHEC biofilm inhibitor.Procaryotes and eucaryotes signal not only themselves but also one another; hence, there is competition and interference of cell signals. For example, interference of acylhomoserine lactones (AHLs) is manifested by AHL lactonases and acylases, which are present in both gram-positive and gram-negative bacteria (79). Similarly, autoinducer-2 (AI-2), a furanosyl borate diester or derivative (39), may be manipulated by Escherichia coli and Vibrio harveyi to interfere with the ability of each species to assess changes in cell population (75). This competition extends beyond procaryotes, as eucaryotes manipulate the quorum-sensing signals of bacteria, too. For example, algae block bacterial biofilm formation via furanones by controlling both AHL signaling (25) and AI-2 signaling (52), and mammals (including humans) block AHL signaling via lactonase in sera (76). Analogously, bacteria take advantage of eucaryotic signals since enterohemorrhagic E. coli O157:H7 (EHEC) bacteria utilize the human hormones epinephrine and norepinephrine to activate virulence genes (33), and bacteria inter...

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Global analysis of candidate genes important for fitness in a competitive biofilm using DNA-array-based transposon mapping

Cited by 33 publications

References 70 publications

RscS Functions Upstream of SypG To Control the syp Locus and Biofilm Formation in Vibrio fischeri

RscS Functions Upstream of SypG To Control the syp Locus and Biofilm Formation in Vibrio fischeri

Escherichia coli NsrR Regulates a Pathway for the Oxidation of 3-Nitrotyramine to 4-Hydroxy-3-Nitrophenylacetate

EnterohemorrhagicEscherichia coliBiofilms Are Inhibited by 7-Hydroxyindole and Stimulated by Isatin

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