Staphylococcus aureus bacteria, including the drug-resistant MRSA, rapidly dismantle their own messenger RNA molecules to switch which proteins they make, helping them dodge the human immune system during infection. This matters because MRSA causes life-threatening skin and respiratory infections that are becoming harder to treat as antibiotics lose effectiveness. The bacteria’s ability to quickly remove old mRNA and control which mRNA gets translated into proteins is central to its success as a pathogen, yet the molecular details of this process remain largely unknown. The researchers aim to map the post-transcriptional regulatory networks that govern this mRNA turnover and translation control in S. aureus, using techniques they have developed over years of work. If successful, this fundamental science will provide detailed molecular insights into a mechanism that is crucial for the bacterium’s survival during infection. While the work is curiosity-driven and has no immediate practical application, understanding these regulatory networks could eventually reveal new molecular targets for drugs that disable the bacteria’s ability to adapt—potentially opening a fresh avenue for treating infections that currently resist existing antibiotics.
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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.
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