YmoA negatively controls the expression of insecticidal genes in Yersinia enterocolitica. Issue 2 (13th March 2014)

• Record Type: Journal Article
• Authors: Starke, Mandy; Fuchs, Thilo M.
• Is Part Of: Molecular microbiology. Volume 92:Issue 2(2014)
• Page Start: 287
• Page End: 301
• Publication Date: 2014-03-13
• Subjects: Molecular microbiology -- Periodicals; 572.829
• DOI: 10.1111/mmi.12554
• Languages: English
• ISSNs: 0950-382X

Abstract

<abstract abstract-type="main"> <title>Summary</title> <p> <italic>Y</italic> <italic>ersinia enterocolitica</italic> is toxic towards invertebrates due to the presence of the toxin complex (<italic>tc</italic>) genes that are activated by the thermolabile regulator TcaR2. In the search for further regulatory factors involved in insecticidal gene expression, the modulator of yersinial virulence, YmoA, was identified to silence all <italic>tc</italic> genes of the <italic>Y</italic><italic>. enterocolitica</italic> strain W22703 (biovar 2, serovar O:9). Using promoter fusions with the luciferase reporter, we found that the deletion of <italic>ymoA</italic> results in elevated transcription of <italic>tcaR1</italic>, <italic>tcaR2</italic>, <italic>tcaA</italic>, <italic>tcaB</italic>, <italic>tcaC</italic>, <italic>tccC1</italic> and <italic>tccC2</italic> at both 15°C and 37°C. Complementation by episomal <italic>ymoA</italic> significantly reduced <italic>tc</italic> gene expression, thus validating the inhibitory activity of YmoA on the production of insecticidal proteins. YmoA contributes to the binding properties of H‐NS to the <italic>tc</italic> promoters by forming a complex with this nucleoid‐associated protein, and this complex not only binds to the upstream regions of all <italic>tc</italic> genes, but also to intragenic sites of <italic>tcaA</italic> and <italic>tcaB</italic> that play an important role in controlling the expression of both genes. At low temperature, the intracellular amount of thermostable YmoA is not reduced, but the repressor is less functional. These data point to H‐NS/YmoA as an antagonist of the inducer TcaR2.</p> </abstract>