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Comparative analysis of the regulation of rovA from the pathogenic yersiniae.
J Bacteriol. 2007 Aug; 189(16):5963-75.JB

Abstract

RovA is a MarR/SlyA-type regulator that mediates the transcription of inv in Yersinia enterocolitica and Y. pseudotuberculosis. In Y. pseudotuberculosis, rovA transcription is controlled primarily by H-NS and RovA, which bind to similar regions within the rovA promoter. At 37 degrees C, rovA transcription is repressed by H-NS. Transcription of rovA results when RovA relieves H-NS-mediated repression. The region of the rovA promoter that H-NS and RovA bind is not conserved in the Y. enterocolitica promoter. Using green fluorescent protein reporters, we determined that the Y. enterocolitica rovA (rovA(Yent)) promoter is weaker than the Y. pseudotuberculosis promoter. However, despite the missing H-NS/RovA binding site in the rovA(Yent) promoter, H-NS and RovA are still involved in the regulation of rovA(Yent). DNA binding studies suggest that H-NS and RovA bind with a higher affinity to the Y. pseudotuberculosis/Y. pestis rovA (rovA(Ypstb/Ypestis)) promoter than to the rovA(Yent) promoter. Furthermore, H-NS appears to bind to two regions in a cooperative fashion within the rovA(Yent) promoter that is not observed with the rovA(Ypstb/Ypestis) promoter. Finally, using a transposon mutagenesis approach, we identified a new positive regulator of rovA in Y. enterocolitica, LeuO. In Escherichia coli, LeuO regulates gene expression via changes in levels of RpoS and H-NS, but LeuO-mediated regulation of rovA(Yent) appears to be independent of either of these two proteins. Together, these data demonstrate that while the rovA regulatory factors are conserved in Yersinia, divergence of Y. enterocolitica and Y. pseudotuberculosis/Y. pestis during evolution has resulted in modifications in the mechanisms that are responsible for controlling rovA transcription.

Authors+Show Affiliations

Washington University School of Medicine, Department of Molecular Microbiology, 660 S. Euclid Avenue, Campus Box 8230, St. Louis, MO 63110, USA. virginia@borcim.wustl.eduNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

17573476

Citation

Lawrenz, Matthew B., and Virginia L. Miller. "Comparative Analysis of the Regulation of rovA From the Pathogenic Yersiniae." Journal of Bacteriology, vol. 189, no. 16, 2007, pp. 5963-75.
Lawrenz MB, Miller VL. Comparative analysis of the regulation of rovA from the pathogenic yersiniae. J Bacteriol. 2007;189(16):5963-75.
Lawrenz, M. B., & Miller, V. L. (2007). Comparative analysis of the regulation of rovA from the pathogenic yersiniae. Journal of Bacteriology, 189(16), 5963-75.
Lawrenz MB, Miller VL. Comparative Analysis of the Regulation of rovA From the Pathogenic Yersiniae. J Bacteriol. 2007;189(16):5963-75. PubMed PMID: 17573476.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Comparative analysis of the regulation of rovA from the pathogenic yersiniae. AU - Lawrenz,Matthew B, AU - Miller,Virginia L, Y1 - 2007/06/15/ PY - 2007/6/19/pubmed PY - 2007/11/8/medline PY - 2007/6/19/entrez SP - 5963 EP - 75 JF - Journal of bacteriology JO - J Bacteriol VL - 189 IS - 16 N2 - RovA is a MarR/SlyA-type regulator that mediates the transcription of inv in Yersinia enterocolitica and Y. pseudotuberculosis. In Y. pseudotuberculosis, rovA transcription is controlled primarily by H-NS and RovA, which bind to similar regions within the rovA promoter. At 37 degrees C, rovA transcription is repressed by H-NS. Transcription of rovA results when RovA relieves H-NS-mediated repression. The region of the rovA promoter that H-NS and RovA bind is not conserved in the Y. enterocolitica promoter. Using green fluorescent protein reporters, we determined that the Y. enterocolitica rovA (rovA(Yent)) promoter is weaker than the Y. pseudotuberculosis promoter. However, despite the missing H-NS/RovA binding site in the rovA(Yent) promoter, H-NS and RovA are still involved in the regulation of rovA(Yent). DNA binding studies suggest that H-NS and RovA bind with a higher affinity to the Y. pseudotuberculosis/Y. pestis rovA (rovA(Ypstb/Ypestis)) promoter than to the rovA(Yent) promoter. Furthermore, H-NS appears to bind to two regions in a cooperative fashion within the rovA(Yent) promoter that is not observed with the rovA(Ypstb/Ypestis) promoter. Finally, using a transposon mutagenesis approach, we identified a new positive regulator of rovA in Y. enterocolitica, LeuO. In Escherichia coli, LeuO regulates gene expression via changes in levels of RpoS and H-NS, but LeuO-mediated regulation of rovA(Yent) appears to be independent of either of these two proteins. Together, these data demonstrate that while the rovA regulatory factors are conserved in Yersinia, divergence of Y. enterocolitica and Y. pseudotuberculosis/Y. pestis during evolution has resulted in modifications in the mechanisms that are responsible for controlling rovA transcription. SN - 0021-9193 UR - https://www.unboundmedicine.com/medline/citation/17573476/Comparative_analysis_of_the_regulation_of_rovA_from_the_pathogenic_yersiniae_ L2 - http://jb.asm.org/cgi/pmidlookup?view=long&pmid=17573476 DB - PRIME DP - Unbound Medicine ER -