Journal
NUCLEIC ACIDS RESEARCH
Volume 42, Issue 17, Pages 10987-10999Publisher
OXFORD UNIV PRESS
DOI: 10.1093/nar/gku790
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Funding
- Sysmo2 Grant (Noisy Strep)
- European Research Council [337399-PneumoCell, ERC-2007-StG 202994-MTP]
- Netherlands Organisation for Scientific Research (NWO-ALW VIDI) [864.12.001]
- UK Biotechnology and Biological Sciences Research Council
- NWO
- Biotechnology and Biological Sciences Research Council [BB/J006378/1, BB/I004564/1] Funding Source: researchfish
- BBSRC [BB/I004564/1, BB/J006378/1] Funding Source: UKRI
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Transcription by RNA polymerase may be interrupted by pauses caused by backtracking or misincorporation that can be resolved by the conserved bacterial Gre-factors. However, the consequences of such pausing in the living cell remain obscure. Here, we developed molecular biology and transcriptome sequencing tools in the human pathogen Streptococcus pneumoniae and provide evidence that transcription elongation is rate-limiting on highly expressed genes. Our results suggest that transcription elongation may be a highly regulated step of gene expression in S. pneumoniae. Regulation is accomplished via long-living elongation pauses and their resolution by elongation factor GreA. Interestingly, mathematical modeling indicates that long-living pauses cause queuing of RNA polymerases, which results in 'transcription traffic jams' on the gene and thus blocks its expression. Together, our results suggest that long-living pauses and RNA polymerase queues caused by them are a major problem on highly expressed genes and are detrimental for cell viability. The major and possibly sole function of GreA in S. pneumoniae is to prevent formation of backtracked elongation complexes.
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