Shedding light on betL*: pPL2-lux mediated real-time analysis of betL* expression in Listeria monocytogenes

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*.