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 Xu, J.
Right arrow Articles by Koudelka, G. B.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Xu, J.
Right arrow Articles by Koudelka, G. B.

 Previous Article  |  Next Article 

Journal of Bacteriology, June 2000, p. 3165-3174, Vol. 182, No. 11
0021-9193/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Mutually Exclusive Utilization of PR and PRM Promoters in Bacteriophage 434 OR

Jian Xu and Gerald B. Koudelka*

Department of Biological Sciences, State University of New York at Buffalo, Buffalo, New York 14260

Received 13 August 1999/Accepted 15 March 2000

Establishment and maintenance of a lysogen of the lambdoid bacteriophage 434 require that the 434 repressor both activate transcription from the PRM promoter and repress transcription from the divergent PR promoter. Several lines of evidence indicate that the 434 repressor activates initiation of PRM transcription by occupying a binding site adjacent to the PRM promoter and directly contacting RNA polymerase. The overlapping architecture of the PRM and PR promoters suggests that an RNA polymerase bound at PR may repress PRM transcription initiation. Hence, part of the stimulatory effect of the 434 repressor may be relief of interference between RNA polymerase binding to the PRM promoter and to the PR promoter. Consistent with this proposal, we show that the repressor cannot activate PRM transcription if RNA polymerase binds at PR prior to addition of the 434 repressor. However, unlike the findings with the related lambda  phage, formation of RNA polymerase promoter complexes at PRM and at PR apparently are mutually exclusive. We find that the RNA polymerase-mediated inhibition of repressor-stimulated PRM transcription requires the presence of an open complex at PR. Taken together, these results indicate that establishment of an open complex at PR directly prevents formation of an RNA polymerase-PRM complex.


* Corresponding author. Mailing address: Department of Biological Sciences, Cooke Hall, North Campus, State University of New York at Buffalo, Buffalo, NY 14260-1300. Phone: (716) 645-3489. Fax: (716) 645-2975. E-mail: koudelka{at}acsu.buffalo.edu.


Journal of Bacteriology, June 2000, p. 3165-3174, Vol. 182, No. 11
0021-9193/00/$04.00+0
Copyright © 2000, 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 © 2000 by the American Society for Microbiology. All rights reserved.