JB
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Neufing, P. J.
Right arrow Articles by Egan, J. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Neufing, P. J.
Right arrow Articles by Egan, J. B.

 Previous Article  |  Next Article 

Journal of Bacteriology, April 2001, p. 2376-2379, Vol. 183, No. 7
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.7.2376-2379.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Establishing Lysogenic Transcription in the Temperate Coliphage 186

Petra J. Neufing,dagger Keith E. Shearwin, and J. Barry Egan*

Department of Molecular Biosciences, Adelaide University, South Australia 5005, Australia

Received 8 June 2000/Accepted 10 January 2001

A single-copy chromosomal reporter system was used to measure the intrinsic strengths and interactions between the three promoters involved in the establishment of lysogeny by coliphage 186. The maintenance lysogenic promoter pL for the immunity repressor gene cI is intrinsically ~20-fold weaker than the lytic promoter pR. These promoters are arranged face-to-face, and transcription from pL is further weakened some 14-fold by the activity of pR. Efficient establishment of lysogeny requires the pE promoter, which lies upstream of pL and is activated by the phage CII protein to a level comparable to that of pR. Transcription of pE is less sensitive to converging pR transcription and raises cI transcription at least 55-fold. The pE promoter does not occlude pL but inhibits lytic transcription by 50%. This interference is not due to bound CII preventing elongation of the lytic transcript. The pE RNA is antisense to the anti-immune repressor gene apl, but any role of this in the establishment of lysogeny appears to be minimal.


* Corresponding author. Mailing address: Department of Molecular Biosciences, Adelaide University, South Australia 5005, Australia. Phone: 61 8 8303 5361. Fax: 61 8 8303 4348. E-mail: barry.egan{at}adelaide.edu.au.

dagger Present address: School of Medicine, Flinders Medical Centre, Flinders University, Bedford Park, South Australia 5042, Australia.


Journal of Bacteriology, April 2001, p. 2376-2379, Vol. 183, No. 7
0021-9193/01/$04.00+0   DOI: 10.1128/JB.183.7.2376-2379.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
Appl. Environ. Microbiol. Infect. Immun. Eukaryot. Cell
Mol. Cell. Biol. J. Virol. Microbiol. Mol. Biol. Rev.
ALL ASM JOURNALS

Copyright © 2001 by the American Society for Microbiology. All rights reserved.