In the food-borne pathogen
Johansson et al. observed that the UTR preceding prfA formed a secondary structure, masking the ribosome-binding region. This structure could switch between an active form at high temperatures, and an inactive form at low temperatures. Mutations predicted to destabilize this structure led to virulence gene expression and invasion of mammalian cells at 30°C. In addition, when DNA corresponding to the UTR was fused to a fluorescent marker in E. coli, the bacteria became fluorescent at 37°C, but not ...