A |[sigma]|-core interaction of the RNA polymerase holoenzyme that enhances promoter escape

doi:doi:10.1038/sj.emboj.7601612

Article

The EMBO Journal (2007) 26, 1579 - 1590
doi:10.1038/sj.emboj.7601612

Published online: 1 March 2007

Subject Category:
- Chromatin and Transcription

A -core interaction of the RNA polymerase holoenzyme that enhances promoter escape

Mark Leibman¹ and Ann Hochschild¹

Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, MA, USA

Correspondence to:

Ann Hochschild, Department of Microbiology and Molecular Genetics, Harvard Medical School, 200 Longwood Ave., D1, Boston, MA 02115, USA. Tel.: +1 617 432 1986; Fax: +1 617 738 7664; E-mail: ahochschild@hms.harvard.edu

Received 2 October 2006; Accepted 24 January 2007

The sigma subunit of bacterial RNA polymerase (RNAP) is required for promoter-specific transcription initiation and can also participate in downstream events. Several functionally important intersubunit interactions between Escherichia coli sigma ⁷⁰ and the core enzyme ( alpha ₂ beta beta ' omega ) have been defined. These include an interaction between conserved region 2 of sigma ⁷⁰ ( sigma ₂) and the coiled-coil domain of beta ' ( beta ' coiled-coil) that is required for sequence-specific interaction between sigma ₂ and the DNA during both promoter open complex formation and sigma ⁷⁰-dependent early elongation pausing. Here, we describe a previously uncharacterized interaction between a region of sigma ⁷⁰ adjacent to sigma ₂ called the nonconserved region ( sigma ⁷⁰ NCR) and a region in the N-terminal portion of beta ' that appears to functionally antagonize the sigma ₂/ beta ' coiled-coil interaction. Specifically, we show that the sigma ⁷⁰ NCR/ beta ' interaction facilitates promoter escape and hinders early elongation pausing, in contrast to the sigma ₂/ beta ' coiled-coil interaction, which has opposite effects. We also demonstrate that removal of the sigma ⁷⁰ NCR results in a severe growth defect; we suggest that its importance for growth may reflect its role in promoter escape.