Send to

Choose Destination
See comment in PubMed Commons below
Mol Microbiol. 2009 Oct;74(2):421-35. doi: 10.1111/j.1365-2958.2009.06874.x. Epub 2009 Oct 1.

Transcriptional and post-transcriptional regulation of the GmaR antirepressor governs temperature-dependent control of flagellar motility in Listeria monocytogenes.

Author information

Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA 02115-6092, USA.


Flagellar motility in Listeria monocytogenes (Lm) is restricted to temperatures below 37 degrees C due to the opposing activities of the MogR transcriptional repressor and the GmaR antirepressor. Previous studies have suggested that both the DegU response regulator and MogR regulate expression of GmaR. In this report, we further define the role of DegU for GmaR production and flagellar motility. We demonstrate that deletion of the receiver domain of DegU has no effect on flagellar motility in Lm. Using transcriptional reporter fusions, we determined that gmaR is cotranscribed within an operon initiating with fliN. Furthermore, the fliN-gmaR promoter (p(fliN-gmaR)) is transcriptionally activated by DegU and is also MogR-repressed. DNA affinity purification, gel mobility shift and footprinting analyses revealed that both DegU and MogR directly bind fliN-gmaR promoter region DNA and that the binding sites do not overlap. Quantitative analysis of gmaR transcripts in Delta mogR bacteria indicated that transcriptional activation of p(fliN-gmaR) by DegU is not inherently temperature-dependent. However, GmaR protein was not detectable at 37 degrees C in Delta mogR bacteria, indicating that a temperature-dependent, post-transcriptional mechanism limits GmaR production to temperatures below 37 degrees C. Our findings reveal that flagellar motility in Lm is governed by both temperature-dependent transcriptional and post-transcriptional regulation of the GmaR antirepressor.

[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Wiley Icon for PubMed Central
    Loading ...
    Support Center