Article

  • The EMBO Journal (2006) 25, 1700 - 1709
  • doi:10.1038/sj.emboj.7601069

Published online: 6 April 2006

The role of an upstream promoter interaction in initiation of bacterial transcription

Sergei Nechaev1,2 and E Peter Geiduschek1

  1. Division of Biological Sciences and Center for Molecular Genetics, University of California, San Diego, La Jolla, CA, USA
  2. Present address: Laboratory of Molecular Carcinogenesis, National Institute of Environmental Health Sciences, 111, TW Alexander Drive, Room D454A, Research Triangle Park, NC 27709, USA

Correspondence to:

Sergei Nechaev, Division of Biological Sciences and Center for Molecular Genetics, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0634, USA. Tel.: +1 858 534 2451; Fax: +1 858 534 7073; E-mail: netchaev@biomail.ucsd.edu

Received 5 January 2006; Accepted 9 March 2006


The bacterial RNA polymerase (RNAP) recognizes promoters through sequence-specific contacts of its promoter-specificity components (sigma) with two DNA sequence motifs. Contacts with the upstream ('-35') promoter motif are made by sigma domain 4 attached to the flap domain of the RNAP beta subunit. Bacteriophage T4 late promoters consist solely of an extended downstream ('-10') motif specifically recognized by the T4 gene 55 protein (gp55). Low level basal transcription is sustained by gp55-RNAP holoenzyme. The late transcription coactivator gp33 binds to the beta flap and represses this basal transcription. Gp33 can also repress transcription by Escherichia coli sigma70-RNAP holoenzyme mutated to allow gp33 access to the beta flap. We propose that repression is due to gp33 blocking an upstream sequence-independent DNA-binding site on RNAP (as sigma70 domain 4 does) but, unlike sigma70 domain 4, providing no new DNA interaction. We show that this upstream interaction is essential only at an early step of transcription initiation, and discuss the role of this interaction in promoter recognition and transcriptional regulation.

  • Keywords:

    • gene regulation,
    • repression,
    • RNA polymerase,
    • phage T4 gp33,
    • promoter
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