This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Mirkin, E. V. Articles by Mirkin, S. M. Search for Related Content PubMed PubMed Citation Articles by Mirkin, E. V. Articles by Mirkin, S. M.

 Previous Article  |  Next Article 

Molecular and Cellular Biology, February 2005, p. 888-895, Vol. 25, No. 3
0270-7306/05/$08.00+0     doi:10.1128/MCB.25.3.888-895.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Mechanisms of Transcription-Replication Collisions in Bacteria

Department of Biochemistry and Molecular Genetics, University of Illinois at Chicago, Chicago, Illinois

Received 22 June 2004/ Returned for modification 22 October 2004/ Accepted 1 November 2004

While collisions between replication and transcription in bacteria are deemed inevitable, the fine details of the interplay between the two machineries are poorly understood. In this study, we evaluate the effects of transcription on the replication fork progression in vivo, by using electrophoresis analysis of replication intermediates. Studying Escherichia coli plasmids, which carry constitutive or inducible promoters in different orientations relative to the replication origin, we show that the mutual orientation of the two processes determines their mode of interaction. Replication elongation appears not to be affected by transcription proceeding in the codirectional orientation. Head-on transcription, by contrast, leads to severe inhibition of the replication fork progression. Furthermore, we evaluate the mechanism of this inhibition by limiting the area of direct contact between the two machineries. We observe that replication pausing zones coincide exactly with transcribed DNA segments. We conclude, therefore, that the replication fork is most likely attenuated upon direct physical interaction with the head-on transcription machinery.

This article has been cited by other articles:

• Hyvarinen, A. K., Pohjoismaki, J. L. O., Reyes, A., Wanrooij, S., Yasukawa, T., Karhunen, P. J., Spelbrink, J. N., Holt, I. J., Jacobs, H. T. (2007). The mitochondrial transcription termination factor mTERF modulates replication pausing in human mitochondrial DNA. Nucleic Acids Res 35: 6458-6474 [Abstract] [Full Text]  
• Wang, J. D., Berkmen, M. B., Grossman, A. D. (2007). Genome-wide coorientation of replication and transcription reduces adverse effects on replication in Bacillus subtilis. Proc. Natl. Acad. Sci. USA 104: 5608-5613 [Abstract] [Full Text]  
• Mirkin, E. V., Mirkin, S. M. (2007). Replication Fork Stalling at Natural Impediments. Microbiol. Mol. Biol. Rev. 71: 13-35 [Abstract] [Full Text]  
• Pohjoismaki, J. L. O., Wanrooij, S., Hyvarinen, A. K., Goffart, S., Holt, I. J., Spelbrink, J. N., Jacobs, H. T. (2006). Alterations to the expression level of mitochondrial transcription factor A, TFAM, modify the mode of mitochondrial DNA replication in cultured human cells. Nucleic Acids Res 34: 5815-5828 [Abstract] [Full Text]  
• Wojciechowska, M., Napierala, M., Larson, J. E., Wells, R. D. (2006). Non-B DNA Conformations Formed by Long Repeating Tracts of Myotonic Dystrophy Type 1, Myotonic Dystrophy Type 2, and Friedreich's Ataxia Genes, Not the Sequences per se, Promote Mutagenesis in Flanking Regions. J. Biol. Chem. 281: 24531-24543 [Abstract] [Full Text]  
• Mirkin, E. V., Castro Roa, D., Nudler, E., Mirkin, S. M. (2006). Transcription regulatory elements are punctuation marks for DNA replication. Proc. Natl. Acad. Sci. USA 103: 7276-7281 [Abstract] [Full Text]