A novel mechanism of translational regulation in bacteria: de-repression of non-canonical start codons in response to oxidative stress

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The harmless soil bacteria called streptomycetes are vital to human welfare because they are the source of the vast majority of antibiotics used by doctors to cure infectious diseases, as well as providing us with numerous other medicines used, for example, to treat cancer, and to help organ transplant patients. We have identified a master regulator (called a 'transcription factor') that switches the genetic machinery of these useful bacteria to allow them to survive in the presence of toxic molecules called Reactive Oxygen Species (a condition called "oxidative stress"). The aim of this work is to find out exactly how the activity of this master regulator is controlled at the molecular level. We also know that this same master regulator controls resistance to oxidative stress in the pathogens Mycobacterium tuberculosis and Corynebacterium diphtheriae, the bacteria that cause the fatal diseases tuberculosis and diphtheria, respectively. This is important because white blood cells ingest pathogenic bacteria and expose them to Reactive Oxygen Species in order to kill them, and so the mechanisms by which disease-causing bacteria like M. tuberculosis and C. diphtheriae resist this oxidative killing are potentially important to human health.