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It takes three for antibiotic resistance

Additional gene suggests new model for regulating methicillin resistance in Staphylococcus aureus

Oeiras, 16.08.12

The central element of methicillin resistance in Staphylococcus aureus is the mecA gene, which in turn is activated in response to the presence of β-lactam antibiotics. The mechanism for this activation was not fully established and some experimental data contradicted the previously accepted model. Now, researchers from the Molecular Genetics Lab in collaboration with researchers at FCT-UNL identified an additional player in the game - a previously unrecognized gene, mecR2 - in addition to the two known regulators. This novel three-component system is presented in the July issue of PLOS Pathogens.

Methicillin-resistance Staphylococcus aureus (MRSA) is a leading cause of hospital acquired infections with an increasingly rising death toll. MRSA strains are resistant to virtually all β-lactam antibiotics (the most common class) and often are also resistant to many other classes of antibiotics, leaving physicians with few therapeutic options. Researchers believe that this work may “pave the way for the design of alternative therapeutic strategies targeting the induction mechanism of the resistance gene”. In addition, the study helps clarifying how antibiotic-resistance has evolved in bacteria.

Original Article

PLoS Pathog 8(7): e1002816. doi:10.1371/journal.ppat.1002816

The Anti-Repressor MecR2 Promotes the Proteolysis of the mecA Repressor and Enables Optimal Expression of β-lactam Resistance in MRSA

Pedro Arêde, Catarina Milheiriço, Hermínia de Lencastre, Duarte C. Oliveira

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