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H-NS mediates the silencing of laterally acquired genes in bacteria.
PLoS Pathog. 2006 Aug; 2(8):e81.PP

Abstract

Histone-like nucleoid structuring protein (H-NS) is a modular protein that is associated with the bacterial nucleoid. We used chromatin immunoprecipitation to determine the binding sites of H-NS and RNA polymerase on the Salmonella enterica serovar Typhimurium chromosome. We found that H-NS does not bind to actively transcribed genes and does not co-localize with RNA polymerase. This shows that H-NS principally silences gene expression by restricting the access of RNA polymerase to the DNA. H-NS had previously been shown to preferentially bind to curved DNA in vitro. In fact, at the genomic level we discovered that the level of H-NS binding correlates better with the AT-content of DNA. This is likely to have evolutionary consequences because we show that H-NS binds to many Salmonella genes acquired by lateral gene transfer, and functions as a gene silencer. The removal of H-NS from the cell causes un-controlled expression of several Salmonella pathogenicity islands, and we demonstrate that this has deleterious consequences for bacterial fitness. Our discovery of this novel role for H-NS may have implications for the acquisition of foreign genes by enteric bacteria.

Authors+Show Affiliations

Molecular Microbiology Group, Institute of Food Research, Colney, Norwich, United Kingdom.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16933988

Citation

Lucchini, Sacha, et al. "H-NS Mediates the Silencing of Laterally Acquired Genes in Bacteria." PLoS Pathogens, vol. 2, no. 8, 2006, pp. e81.
Lucchini S, Rowley G, Goldberg MD, et al. H-NS mediates the silencing of laterally acquired genes in bacteria. PLoS Pathog. 2006;2(8):e81.
Lucchini, S., Rowley, G., Goldberg, M. D., Hurd, D., Harrison, M., & Hinton, J. C. (2006). H-NS mediates the silencing of laterally acquired genes in bacteria. PLoS Pathogens, 2(8), e81.
Lucchini S, et al. H-NS Mediates the Silencing of Laterally Acquired Genes in Bacteria. PLoS Pathog. 2006;2(8):e81. PubMed PMID: 16933988.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - H-NS mediates the silencing of laterally acquired genes in bacteria. AU - Lucchini,Sacha, AU - Rowley,Gary, AU - Goldberg,Martin D, AU - Hurd,Douglas, AU - Harrison,Marcus, AU - Hinton,Jay C D, PY - 2006/05/31/received PY - 2006/07/06/accepted PY - 2006/8/29/pubmed PY - 2006/12/9/medline PY - 2006/8/29/entrez SP - e81 EP - e81 JF - PLoS pathogens JO - PLoS Pathog VL - 2 IS - 8 N2 - Histone-like nucleoid structuring protein (H-NS) is a modular protein that is associated with the bacterial nucleoid. We used chromatin immunoprecipitation to determine the binding sites of H-NS and RNA polymerase on the Salmonella enterica serovar Typhimurium chromosome. We found that H-NS does not bind to actively transcribed genes and does not co-localize with RNA polymerase. This shows that H-NS principally silences gene expression by restricting the access of RNA polymerase to the DNA. H-NS had previously been shown to preferentially bind to curved DNA in vitro. In fact, at the genomic level we discovered that the level of H-NS binding correlates better with the AT-content of DNA. This is likely to have evolutionary consequences because we show that H-NS binds to many Salmonella genes acquired by lateral gene transfer, and functions as a gene silencer. The removal of H-NS from the cell causes un-controlled expression of several Salmonella pathogenicity islands, and we demonstrate that this has deleterious consequences for bacterial fitness. Our discovery of this novel role for H-NS may have implications for the acquisition of foreign genes by enteric bacteria. SN - 1553-7374 UR - https://www.unboundmedicine.com/medline/citation/16933988/H_NS_mediates_the_silencing_of_laterally_acquired_genes_in_bacteria_ L2 - https://dx.plos.org/10.1371/journal.ppat.0020081 DB - PRIME DP - Unbound Medicine ER -