Imperial College London
Alternate

Professor Martin Buck FRS

Faculty of Natural Sciences, Department of Life Sciences

Senior Research Investigator
 
 
 
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Contact

 

+44 (0)20 7594 5442m.buck

 
 
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Location

 

448Sir Alexander Fleming BuildingSouth Kensington Campus

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Summary

 

Publications

Citation

BibTex format

@article{Schaefer:2015:nar/gkv597,
author = {Schaefer, J and Engl, C and Zhang, N and Lawton, E and Buck, M},
doi = {nar/gkv597},
journal = {Nucleic Acids Research},
pages = {7280--7291},
title = {Genome wide interactions of wild-type and activator bypass forms of σ54.},
url = {http://dx.doi.org/10.1093/nar/gkv597},
volume = {43},
year = {2015}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Enhancer-dependent transcription involving the promoter specificity factor σ(54) is widely distributed amongst bacteria and commonly associated with cell envelope function. For transcription initiation, σ(54)-RNA polymerase yields open promoter complexes through its remodelling by cognate AAA+ ATPase activators. Since activators can be bypassed in vitro, bypass transcription in vivo could be a source of emergent gene expression along evolutionary pathways yielding new control networks and transcription patterns. At a single test promoter in vivo bypass transcription was not observed. We now use genome-wide transcription profiling, genome-wide mutagenesis and gene over-expression strategies in Escherichia coli, to (i) scope the range of bypass transcription in vivo and (ii) identify genes which might alter bypass transcription in vivo. We find little evidence for pervasive bypass transcription in vivo with only a small subset of σ(54) promoters functioning without activators. Results also suggest no one gene limits bypass transcription in vivo, arguing bypass transcription is strongly kept in check. Promoter sequences subject to repression by σ(54) were evident, indicating loss of rpoN (encoding σ(54)) rather than creating rpoN bypass alleles would be one evolutionary route for new gene expression patterns. Finally, cold-shock promoters showed unusual σ(54)-dependence in vivo not readily correlated with conventional σ(54) binding-sites.
AU  - Schaefer,J
AU  - Engl,C
AU  - Zhang,N
AU  - Lawton,E
AU  - Buck,M
DO  - nar/gkv597
EP  - 7291
PY  - 2015///
SN  - 1362-4962
SP  - 7280
TI  - Genome wide interactions of wild-type and activator bypass forms of σ54.
T2  - Nucleic Acids Research
UR  - http://dx.doi.org/10.1093/nar/gkv597
UR  - http://hdl.handle.net/10044/1/24451
VL  - 43
ER  -
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