HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Supplementary data Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by van der Veen, S. Articles by Wells-Bennik, M. H. J. Search for Related Content PubMed PubMed Citation Articles by van der Veen, S. Articles by Wells-Bennik, M. H. J. Agricola Articles by van der Veen, S. Articles by Wells-Bennik, M. H. J.

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

Stijn van der Veen^1,2,3,

Torsten Hain^4,

¹ Wageningen Centre for Food Sciences (WCFS), Diedenweg 20, 6703 GW Wageningen, The Netherlands
² Division of Health and Safety, NIZO Food Research, Kernhemseweg 2, 6718 ZB Ede, The Netherlands
³ Laboratory of Food Microbiology, Wageningen University and Research Centre, Bomenweg 2, 6703 HD Wageningen, The Netherlands
⁴ Institute of Medical Microbiology, Justus-Liebig University, Frankfurter Strasse 107, 35392 Giessen, Germany

Correspondence
Stijn van der Veen
Stijn.vanderVeen{at}wur.nl

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 °C and exposed to 48 °C were examined using DNA microarrays. Transcription levels were measured over a 40 min period after exposure of the culture to 48 °C and compared with those of unexposed cultures at 37 °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.

These authors contributed equally to this work.

Supplementary tables of the sequences of the Q-PCR primers and the genes that show differential expression at different time points after exposure to a temperature of 48 °C are available with the online version of this paper.

The microarray platform and microarray data discussed in this publication have been deposited in ArrayExpress (http://www.ebi.ac.uk/arrayexpress) under accession numbers A-MEXP-752 and E-MEXP-1118, respectively.