NusG is an intrinsic transcription termination factor that stimulates motility and coordinates gene expression with NusA
NusA and NusG are transcription factors that stimulate RNA polymerase pausing in Bacillus subtilis. While NusA was known to function as an intrinsic termination factor in B. subtilis, the role of NusG in this process was unknown. To examine the individual and combinatorial roles that NusA and NusG play in intrinsic termination, Term-seq was conducted in wild type, NusA depletion, DnusG, and NusA depletion DnusG strains. We determined that NusG functions as an intrinsic termination factor that works alone and cooperatively with NusA to facilitate termination at 88% of the 1400 identified intrinsic terminators. Our results indicate that NusG stimulates a sequence-specific pause that assists in the completion of suboptimal terminator hairpins with weak terminal A-U and G-U base pairs at the bottom of the stem. Loss of NusA and NusG leads to global misregulation of gene expression and loss of NusG results in flagella and swimming motility defects.
RNA-seq data were deposited in GEO under accession number GSE154522. All other data generated or analysed during this study are included in the manuscript and supporting files.
Article and author information
National Institutes of Health (GM098399)
- Paul Babitzke
National Institutes of Health (GM131783)
- Daniel B Kearns
National Institutes of Health (intramural)
- Mikhail Kashlev
The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.
- Joseph T Wade, Wadsworth Center, New York State Department of Health, United States
- Received: August 7, 2020
- Accepted: April 8, 2021
- Accepted Manuscript published: April 9, 2021 (version 1)
- Version of Record published: April 21, 2021 (version 2)
This is an open-access article, free of all copyright, and may be freely reproduced, distributed, transmitted, modified, built upon, or otherwise used by anyone for any lawful purpose. The work is made available under the Creative Commons CC0 public domain dedication.
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