| Literature DB >> 27212260 |
Shauna M Keane1, Eamonn P Culligan1, Roland F Hoffmann2, Cormac G M Gahan2,3,4, Colin Hill2,3, William J Snelling5, Roy D Sleator1,2.
Abstract
We propose a mechanism of action for the betL* mutation which is based on DNA topology. Removing a single thymine residue from the betL σ(A) promoter's -10 and -35 spacer results in a 'twist'-mediated activation of transcription which accounts for the osmotolerance phenotype observed for strains expressing betL*.Entities:
Keywords: Listeria; betL*; lux; osmotolerance
Mesh:
Substances:
Year: 2016 PMID: 27212260 PMCID: PMC4879987 DOI: 10.1080/21655979.2016.1171438
Source DB: PubMed Journal: Bioengineered ISSN: 2165-5979 Impact factor: 3.269