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Role of operator subsites in Arc repression
1Department of Biology, Massachusetts Institute of Technology, Cambridge 02139, USA.
Journal of Molecular Biology
|November 29, 1996
Summary
Arc repressor binding to bacteriophage P22 operator sites controls transcription of the immunity I operon. A single Arc dimer binding event at a specific operator subsite is sufficient to significantly repress transcription initiation.
Area of Science:
- Molecular Biology
- Genetics
- Virology
Background:
- The Arc repressor regulates transcription of the immunity I operon in bacteriophage P22.
- Arc functions by binding to a 21 base-pair operator controlling two divergent promoters, Pant and Pmnt.
- Arc dimers exhibit nanomolar affinity for operator subsites and utilize protein-protein interactions for stable binding.
Purpose of the Study:
- To investigate the transcriptional repression mechanism of the Arc repressor.
- To determine the role of individual operator subsites in Arc-mediated repression.
- To elucidate how Arc binding affects RNA polymerase open-complex formation.
Main Methods:
- Analysis of Arc repressor binding to single operator subsites.
- Quantification of repression effects on Pant and Pmnt promoter variants.
- Assessment of RNA polymerase open-complex formation rates.
Main Results:
- A single Arc dimer bound to one subsite significantly reduces RNA polymerase open-complex formation.
- Repression efficiency varies depending on which subsite is occupied and the promoter targeted.
- The operator subsite proximal to the Pant -35 region (also the -10 region for Pmnt) is primarily responsible for repression.
Conclusions:
- Arc repressor binding to a single operator subsite is sufficient for significant transcriptional repression.
- Differential binding affinities and positions within the operator dictate repression efficacy for divergent promoters.
- The identified operator subsite plays a crucial role in regulating bacteriophage P22 immunity gene expression.