The ability to adapt to environments of fluctuating nutrient availability is vital for bacterial survival. In response to nitrogen limitation, Mycobacterium tuberculosis alters nitrate/nitrite metabolism, aspartate metabolism and cell wall biosynthesis. GlnR is a key regulator involved in this response, controlling the expression of genes involved in nitric oxide detoxification and intracellular survival, markedly different to the GlnR-mediated nitrogen scavenging response seen in non-pathogenic mycobacteria. This has implications for Tuberculosis (TB) control in terms of designing new drugs to treat infection.
Brian D. Robertson PhD FHEA
MRC Centre for Molecular Bacteriology and Infection