Format

Send to

Choose Destination
See comment in PubMed Commons below
Microbiology. 2007 Oct;153(Pt 10):3593-607.

The heat-shock response of Listeria monocytogenes comprises genes involved in heat shock, cell division, cell wall synthesis, and the SOS response.

Author information

  • 1Wageningen Centre for Food Sciences (WCFS), Diedenweg 20, 6703 GW Wageningen, The Netherlands. Stijn.vanderVeen@wur.nl

Abstract

The food-borne pathogen Listeria monocytogenes has the ability to survive extreme environmental conditions due to an extensive interacting network of stress responses. It is able to grow and survive at relatively high temperatures in comparison with other non-sporulating food-borne pathogens. To investigate the heat-shock response of L. monocytogenes, whole-genome expression profiles of cells that were grown at 37 degrees C and exposed to 48 degrees C were examined using DNA microarrays. Transcription levels were measured over a 40 min period after exposure of the culture to 48 degrees C and compared with those of unexposed cultures at 37 degrees C. After 3 min, 25 % of all genes were differentially expressed, while after 40 min only 2 % of all genes showed differential expression, indicative of the transient nature of the heat-shock response. The global transcriptional response was validated by analysing the expression of a set of 13 genes by quantitative PCR. Genes previously identified as part of the class I and class III heat-shock response and the class II stress response showed induction at one or more of the time points investigated. This is believed to be the first study to report that several heat-shock-induced genes are part of the SOS response in L. monocytogenes. Furthermore, numerous differentially expressed genes that have roles in the cell division machinery or cell wall synthesis were down-regulated. This expression pattern is in line with the observation that heat shock results in cell elongation and prevention of cell division.

[PubMed - indexed for MEDLINE]

LinkOut - more resources

Full Text Sources

Other Literature Sources

PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Ingenta plc
    Loading ...
    Write to the Help Desk