Unravelling post-transcriptional regulatory networks in pathogenic S. aureus

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Antimicrobial medicines have saved millions of lives since the introduction of penicillin in the 1940s. But their overuse has resulted in the rise of multidrug-resistant bacteria at a rate that has outpaced the discovery of new antibiotics. The emergence of multi-drug resistant Staphylococcus aureus (such as MRSA) in particular is causing major healthcare problems world-wide as S. aureus skin and respiratory infections can be life-threatening and are becoming increasingly more difficult to treat. Like all organisms, MRSA initially makes temporary copies of its genes, called messenger RNA (mRNA) molecules, which can subsequently be read, or translated, by a molecular machine called the ribosome to generate proteins. How much of a protein is made depends on how much of its mRNA is present and how well it accesses the translation machinery. Proteins enable the organism to survive and, for bacteria like S. aureus, to infect human cells. One reason why S. aureus is such a successful human pathogen is because it can quickly remove mRNAs that are no longer required and control which mRNAs are translated. This enables the organism to swiftly adapt to challenges from the immune system by changing the proteins that it makes. This mechanism is crucial for S. aureus survival during infection, but we know remarkably little about how it works. The goal of our research is to gain detailed molecular insights into this process, using innovative techniques that we have developed over the years. The results from our studies may help uncover new ways of battling infectious diseases.