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FabR regulates Salmonella biofilm formation via its direct target FabB

Kim Hermans, Stefanie Roberfroid, Inge M Thijs, Gwendoline Kint, David De Coster, Kathleen Marchal UGent, Jos Vanderleyden, Sigrid CJ De Keersmaecker and Hans P Steenackers (2016) BMC GENOMICS. 17.
abstract
Background: Biofilm formation is an important survival strategy of Salmonella in all environments. By mutant screening, we showed a knock-out mutant of fabR, encoding a repressor of unsaturated fatty acid biosynthesis (UFA), to have impaired biofilm formation. In order to unravel how this regulator impinges on Salmonella biofilm formation, we aimed at elucidating the S. Typhimurium FabR regulon. Hereto, we applied a combinatorial high-throughput approach, combining ChIP-chip with transcriptomics. Results: All the previously identified E. coli FabR transcriptional target genes (fabA, fabB and yqfA) were shown to be direct S. Typhimurium FabR targets as well. As we found a fabB overexpressing strain to partly mimic the biofilm defect of the fabR mutant, the effect of FabR on biofilms can be attributed at least partly to FabB, which plays a key role in UFA biosynthesis. Additionally, ChIP-chip identified a number of novel direct FabR targets (the intergenic regions between hpaR/hpaG and ddg/ydfZ) and yet putative direct targets (i.a. genes involved in tRNA metabolism, ribosome synthesis and translation). Next to UFA biosynthesis, a number of these direct targets and other indirect targets identified by transcriptomics (e.g. ribosomal genes, ompA, ompC, ompX, osmB, osmC, sseI), could possibly contribute to the effect of FabR on biofilm formation. Conclusion: Overall, our results point at the importance of FabR and UFA biosynthesis in Salmonella biofilm formation and their role as potential targets for biofilm inhibitory strategies.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
IBCN, Biofilm, Salmonella, FabR, FabB, Unsaturated fatty acids, ChIP-chip, ENTERICA SEROVAR TYPHIMURIUM, FATTY-ACID BIOSYNTHESIS, TRANSCRIPTION FACTOR-BINDING, GENOME-WIDE LOCATION, ESCHERICHIA-COLI, PROTEIN EXPRESSION, GROWTH-CONDITIONS, MEMBRANE, RESISTANCE, GENES
journal title
BMC GENOMICS
BMC Genomics
volume
17
article number
253
pages
15 pages
Web of Science type
Article
Web of Science id
000372544000003
JCR category
BIOTECHNOLOGY & APPLIED MICROBIOLOGY
JCR impact factor
3.729 (2016)
JCR rank
33/158 (2016)
JCR quartile
1 (2016)
ISSN
1471-2164
DOI
10.1186/s12864-016-2387-x
project
Bioinformatics: from nucleotids to networks (N2N)
language
English
UGent publication?
no
classification
A1
copyright statement
I have retained and own the full copyright for this publication
id
7206861
handle
http://hdl.handle.net/1854/LU-7206861
date created
2016-05-11 15:36:35
date last changed
2017-04-27 08:41:28
@article{7206861,
  abstract     = {Background: Biofilm formation is an important survival strategy of Salmonella in all environments. By mutant screening, we showed a knock-out mutant of fabR, encoding a repressor of unsaturated fatty acid biosynthesis (UFA), to have impaired biofilm formation. In order to unravel how this regulator impinges on Salmonella biofilm formation, we aimed at elucidating the S. Typhimurium FabR regulon. Hereto, we applied a combinatorial high-throughput approach, combining ChIP-chip with transcriptomics. 
Results: All the previously identified E. coli FabR transcriptional target genes (fabA, fabB and yqfA) were shown to be direct S. Typhimurium FabR targets as well. As we found a fabB overexpressing strain to partly mimic the biofilm defect of the fabR mutant, the effect of FabR on biofilms can be attributed at least partly to FabB, which plays a key role in UFA biosynthesis. Additionally, ChIP-chip identified a number of novel direct FabR targets (the intergenic regions between hpaR/hpaG and ddg/ydfZ) and yet putative direct targets (i.a. genes involved in tRNA metabolism, ribosome synthesis and translation). Next to UFA biosynthesis, a number of these direct targets and other indirect targets identified by transcriptomics (e.g. ribosomal genes, ompA, ompC, ompX, osmB, osmC, sseI), could possibly contribute to the effect of FabR on biofilm formation. 
Conclusion: Overall, our results point at the importance of FabR and UFA biosynthesis in Salmonella biofilm formation and their role as potential targets for biofilm inhibitory strategies.},
  articleno    = {253},
  author       = {Hermans, Kim and Roberfroid, Stefanie and Thijs, Inge M and Kint, Gwendoline and De Coster, David and Marchal, Kathleen and Vanderleyden, Jos and De Keersmaecker, Sigrid CJ and Steenackers, Hans P},
  issn         = {1471-2164},
  journal      = {BMC GENOMICS},
  keyword      = {IBCN,Biofilm,Salmonella,FabR,FabB,Unsaturated fatty acids,ChIP-chip,ENTERICA SEROVAR TYPHIMURIUM,FATTY-ACID BIOSYNTHESIS,TRANSCRIPTION FACTOR-BINDING,GENOME-WIDE LOCATION,ESCHERICHIA-COLI,PROTEIN EXPRESSION,GROWTH-CONDITIONS,MEMBRANE,RESISTANCE,GENES},
  language     = {eng},
  pages        = {15},
  title        = {FabR regulates Salmonella biofilm formation via its direct target FabB},
  url          = {http://dx.doi.org/10.1186/s12864-016-2387-x},
  volume       = {17},
  year         = {2016},
}

Chicago
Hermans, Kim, Stefanie Roberfroid, Inge M Thijs, Gwendoline Kint, David De Coster, Kathleen Marchal, Jos Vanderleyden, Sigrid CJ De Keersmaecker, and Hans P Steenackers. 2016. “FabR Regulates Salmonella Biofilm Formation via Its Direct Target FabB.” Bmc Genomics 17.
APA
Hermans, Kim, Roberfroid, S., Thijs, I. M., Kint, G., De Coster, D., Marchal, K., Vanderleyden, J., et al. (2016). FabR regulates Salmonella biofilm formation via its direct target FabB. BMC GENOMICS, 17.
Vancouver
1.
Hermans K, Roberfroid S, Thijs IM, Kint G, De Coster D, Marchal K, et al. FabR regulates Salmonella biofilm formation via its direct target FabB. BMC GENOMICS. 2016;17.
MLA
Hermans, Kim, Stefanie Roberfroid, Inge M Thijs, et al. “FabR Regulates Salmonella Biofilm Formation via Its Direct Target FabB.” BMC GENOMICS 17 (2016): n. pag. Print.