Transcriptional and posttranscriptional regulation of Shigella shuT in response to host-associated iron availability and temperature.

Like most bacteria, Shigella must maintain a precise balance between the necessity and toxicity of iron; a balance that is achieved, at least in part, by regulating the production of bacterial iron acquisition systems in response to specific environmental signals. Using the Shigella heme utilization (Shu) system, S. dysenteriae is able to acquire iron from heme, a potentially rich source of nutritional iron within the otherwise iron-limited environment of the human host. Investigations presented within reveal two distinct molecular mechanisms underlying previously uncharacterized transcriptional and translational regulation of shuT, a gene encoding the periplasmic-binding component of the Shu system. While shuT transcription is regulated in response to iron availability via a process dependent upon the global regulator Fur and a Fur-binding site located immediately downstream of the promoter, shuT translation is regulated in response to environmental temperature via the activity of an RNA thermometer located within the 5' untranslated region of the gene. Such complex regulation likely increases the fitness of S. dysenteriae by ensuring maximal ShuT production when the pathogen is within the iron-limited and relatively warm environment of the infected host, the only environment in which heme will be encountered as a potential source of essential iron.