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Disarming disease-causing bacteria

Scientists could produce new antibacterial treatments by disarming the molecular pumps bacteria use to bring disease causing molecules in contact with animals and humans.

Research published today in Nature Structure and Molecular Biology showed a protein complex called the Translocation and Assembly Module (TAM), forms a type of molecular pump, allowing bacteria to shuttle key disease causing molecules from inside the bacterial cell where they are made, to the outside surface, priming the bacteria to infect other organisms.

The international research collaboration, led by Monash University, paves the way for future studies to design new drugs that inhibit this process.

The TAM was discovered in many disease-causing bacteria, from micro-organisms that cause whooping cough and meningitis, to hospital-acquired bacteria that are developing resistance to current antibiotics.

The Monash team, led by Professor Trevor Lithgow from the Department of Biochemistry and Molecular Biology, showed the TAM was made of two protein parts, TamA and TamB, which function together to form a machine of molecular scale.

Lead author and PhD student Joel Selkrig said the team, with colleagues at the University of Melbourne, compared mutant strains of bacteria engineered to have no TAM, to normal virulent bacteria.

"We noticed that proteins important for disease were missing in the outer membrane of the mutant bacteria," Mr Selkrig said.

"The missing proteins help the bacteria to adhere to our bodies and perform disease-related functions."

Mr Selkrig said the next step for the group was to dissect the molecular mechanism of how the TAM complex functions and, in collaboration with researchers at the Monash Institute of Pharmaceutical Sciences, design an antibiotic that inhibits the TAM in bacteria.

"The TAM is a good antibacterial target because a drug designed to inhibit TAM function would not kill bacteria, it would simply deprive them of their molecular weaponry, and in doing so, disable the disease process," Mr Selkrig said.

"By allowing bacteria to stay alive after antibiotic treatment, we believe we can also prevent the emergence of antibiotic resistance, which is fast-becoming a major problem worldwide."

Professor Lithgow led a team of seven Monash researchers, and scientists from the University of Melbourne, University of Queensland, the University of Glasgow and University of Birmingham.


Contact: Emily Walker
Monash University

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