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Journal of Bacteriology, April 2005, p. 2592-2600, Vol. 187, No. 8
0021-9193/05/$08.00+0     doi:10.1128/JB.187.8.2592-2600.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Expression of the bmpB Gene of Borrelia burgdorferi Is Modulated by Two Distinct Transcription Termination Events

Ramesh Ramamoorthy,* Natalie A. McClain, Aarti Gautam, and Dorothy Scholl-Meeker

Division of Bacteriology and Parasitology, Tulane National Primate Research Center, Tulane University Health Sciences Center, Covington, Louisiana

Received 4 September 2004/ Accepted 12 January 2005

bmp gene family 36 of Borrelia burgdorferi, the agent of Lyme disease, comprises four paralogs: bmpA, bmpB, bmpC, and bmpD. The bmpA and bmpB genes constitute an operon. All four genes have been found to be transcribed in cultured spirochetes. Expression from the bmpAB operon results in three distinct transcripts of 1.1, 1.6, and 2.4 kb, and the relative expression of bmpA mRNA is three- to fourfold greater than that of bmpB mRNA. However, thus far only expression of the BmpA protein has been demonstrated. Therefore, in this study we characterized the origins of the three transcripts and compared the relative expression of the BmpA and BmpB proteins. Northern blotting revealed that the three distinct transcripts originated from a single promoter located upstream of bmpA but terminated either 3' to the bmpA (1.1-kb RNA) or bmpB (2.4-kb RNA) gene or, most unusually, within the bmpB gene (1.6-kb RNA). Termination within the bmpB gene was associated with a functional Rho-independent transcription terminator. At the protein level, we also observed a 4.3-fold greater abundance of BmpA compared to that of BmpB. These studies identify a transcription termination mechanism in B. burgdorferi resulting in the disparate expression of the two genes of the bmpAB operon.

* Corresponding author. Mailing address: Division of Bacteriology and Parasitology, 18703 Three Rivers Rd., Covington, LA 70433. Phone: (985) 871-6361. Fax: (985) 871-6390. E-mail: rramesh{at}tulane.edu.

Journal of Bacteriology, April 2005, p. 2592-2600, Vol. 187, No. 8
0021-9193/05/$08.00+0     doi:10.1128/JB.187.8.2592-2600.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Ramesh, G., Borda, J. T., Dufour, J., Kaushal, D., Ramamoorthy, R., Lackner, A. A., Philipp, M. T. (2008). Interaction of the Lyme Disease Spirochete Borrelia burgdorferi with Brain Parenchyma Elicits Inflammatory Mediators from Glial Cells as Well as Glial and Neuronal Apoptosis. Am. J. Pathol. 173: 1415-1427 [Abstract] [Full Text]  
  • Pal, U., Wang, P., Bao, F., Yang, X., Samanta, S., Schoen, R., Wormser, G. P., Schwartz, I., Fikrig, E. (2008). Borrelia burgdorferi basic membrane proteins A and B participate in the genesis of Lyme arthritis. JEM 205: 133-141 [Abstract] [Full Text]  
  • Gautam, A., Hathaway, M., McClain, N., Ramesh, G., Ramamoorthy, R. (2008). Analysis of the determinants of bba64 (P35) gene expression in Borrelia burgdorferi using a gfp reporter. Microbiology 154: 275-285 [Abstract] [Full Text]  


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