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      The transcriptional programme of Salmonella enterica serovar Typhimurium reveals a key role for tryptophan metabolism in biofilms

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          Biofilm formation enhances the capacity of pathogenic Salmonella bacteria to survive stresses that are commonly encountered within food processing and during host infection. The persistence of Salmonella within the food chain has become a major health concern, as biofilms can serve as a reservoir for the contamination of food products. While the molecular mechanisms required for the survival of bacteria on surfaces are not fully understood, transcriptional studies of other bacteria have demonstrated that biofilm growth triggers the expression of specific sets of genes, compared with planktonic cells. Until now, most gene expression studies of Salmonella have focused on the effect of infection-relevant stressors on virulence or the comparison of mutant and wild-type bacteria. However little is known about the physiological responses taking place inside a Salmonella biofilm.


          We have determined the transcriptomic and proteomic profiles of biofilms of Salmonella enterica serovar Typhimurium. We discovered that 124 detectable proteins were differentially expressed in the biofilm compared with planktonic cells, and that 10% of the S. Typhimurium genome (433 genes) showed a 2-fold or more change in the biofilm compared with planktonic cells. The genes that were significantly up-regulated implicated certain cellular processes in biofilm development including amino acid metabolism, cell motility, global regulation and tolerance to stress. We found that the most highly down-regulated genes in the biofilm were located on Salmonella Pathogenicity Island 2 (SPI2), and that a functional SPI2 secretion system regulator ( ssrA) was required for S. Typhimurium biofilm formation. We identified STM0341 as a gene of unknown function that was needed for biofilm growth. Genes involved in tryptophan ( trp) biosynthesis and transport were up-regulated in the biofilm. Deletion of trpE led to decreased bacterial attachment and this biofilm defect was restored by exogenous tryptophan or indole.


          Biofilm growth of S. Typhimurium causes distinct changes in gene and protein expression. Our results show that aromatic amino acids make an important contribution to biofilm formation and reveal a link between SPI2 expression and surface-associated growth in S. Typhimurium.

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          Most cited references 94

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          Aromatic-dependent Salmonella typhimurium are non-virulent and effective as live vaccines.

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            Exploring the Metabolic and Genetic Control of Gene Expression on a Genomic Scale

             J. L. DeRisi (1997)
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              Genetic analysis of Escherichia coli biofilm formation: roles of flagella, motility, chemotaxis and type I pili.

              We have used Escherichia coli as a model system to investigate the initiation of biofilm formation. Here, we demonstrate that E. coli forms biofilms on multiple abiotic surfaces in a nutrient-dependent fashion. In addition, we have isolated insertion mutations that render this organism defective in biofilm formation. One-half of these mutations was found to perturb normal flagellar function. Using defined fli, flh, mot and che alleles, we show that motility, but not chemotaxis, is critical for normal biofilm formation. Microscopic analyses of these mutants suggest that motility is important for both initial interaction with the surface and for movement along the surface. In addition, we present evidence that type I pili (harbouring the mannose-specific adhesin, FimH) are required for initial surface attachment and that mannose inhibits normal attachment. In light of the observations presented here, a working model is discussed that describes the roles of both motility and type I pili in biofilm development.

                Author and article information

                BMC Genomics
                BMC Genomics
                BioMed Central
                11 December 2009
                : 10
                : 599
                [1 ]Institute of Food Research, Norwich Research Park, Colney, Norwich, NR4 7UA, UK
                [2 ]Department of Biological Sciences, University of Exeter, Exeter, EX4 4PS, UK
                [3 ]National Laboratory Service, Starcross Laboratory, Staplake Mount, Starcross, EX6 8PE, UK
                [4 ]School of Biological Sciences, University of Southampton, Southampton, SO16 7PX, UK
                [5 ]Department of Microbiology, School of Genetics & Microbiology, Moyne Institute of Preventive Medicine, Trinity College, Dublin 2, Ireland
                [6 ]Shea Hamilton, Faculty of Medicine, Imperial College London, Norfolk Place, London, W2 1PG, UK; Brett Cochrane, Unilever SEAC, Colworth Science Park, Sharnbrook, Bedfordshire, MK44 1LQ, UK
                Copyright ©2009 Hamilton et al; licensee BioMed Central Ltd.

                This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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