Pseudomonas aeruginosa is a model organism that can provide insight into gene regulation in other microbes, including pathogens. P. aeruginosa is found in a wide variety of environmental niches and is an opportunistic human pathogen capable of causing serious bacterial infections. Its environmental adaptability is reflected in its genome, which contains many systems for iron uptake. Iron is a metal ion required by all living cells, as it is an essential cofactor for many important proteins.
P. aeruginosa synthesises siderophores for iron uptake, but can also scavenge exogenous siderophores made by other microorganisms and can uptake these to gain iron in iron-depriving conditions. One type of iron uptake systems are cell surface signalling (CSS) systems, which control the uptake of iron bound to siderophores, compounds that chelate iron efficiently. CSS systems generally comprise an outer membrane receptor, transmembrane sigma regulator, and a sigma factor that directs expression of iron uptake genes via interaction with RNA polymerase.
This study focussed on understanding how CSS systems for the uptake of exogenous siderophores desferrioxamine and ferrichrome of P. aeruginosa achieve iron uptake. The foxIR genes encode a s regulator/s pair of proteins that respond to the uptake of ferrioxamine through the FoxA outer membrane receptor protein. The fiuIR genes encode a similar pair of s regulator/s proteins that respond to and coordinate uptake of ferrichrome through the FiuA outer membrane receptor.
This study used a combination of constructing gene knockouts, reporter gene assays to quantify target gene expression / activity of the sigma factors, and analysis of protein presence and amount by Western blot. The two exogenous ECFs systems studied revealed striking differences, despite similarities in their components and genomic architecture. These differences highlight the specificity of the individual systems despite their apparent similarity. ECFs are important potential future tools for biotechnology, so understanding their specificity and molecular mechanisms of activation and gene response is critical.