In 2013, there was an outbreak of methicillin-resistant Staphylococcus aureus (MRSA) at an NFL training facility. One player suffered a career-ending infection to his foot and sued the team owners for $20 million for unsanitary conditions that contributed to the bacterial infection. A settlement with undisclosed terms was reached in 2017. MRSA is highly contagious and is spread by direct skin contact or by airborne transmission and can result in amputation or death. In addition, MRSA is very difficult to treat because it is resistant to many antibiotics. For example, β-lactamβ-lactam antibiotics, such as penicillin, function by binding to and inactivating bacterial penicillin-binding proteins (PBPs), which synthesize the bacterial cell wall. However, MRSA expresses an alternative type of PBP, called PBP2a encoded by the mecA gene. β-lactamβ-lactam antibiotics only weakly bind PBP2a, and thus cell wall synthesis can continue in their presence. Moreover, in a system somewhat analogous to the regulation of the lac operon, mecA is induced by the presence of β-lactamβ-lactam antibiotics and repressed in their absence. This “on-demand” expression of mecA means that when the infection is treated with antibiotics, the cells ramp up their resistance. 1. Chen et al. [Antimicrob. Agents Chemother. (2014) 58(2):1047–1054] studied several strains of MRSA isolated in Taiwan and found that some single point mutations in the mecA promoter were linked to increased antibiotic resistance while other point mutations were linked to decreased antibiotic resistance. Why might mecA promoter mutations have these opposing effects?

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In 2013, there was an outbreak of methicillin-resistant Staphylococcus aureus (MRSA) at an NFL training facility. One player suffered a career-ending infection to his foot and sued the team owners for $20 million for unsanitary conditions that contributed to the bacterial infection. A settlement with undisclosed terms was reached in 2017. MRSA is highly contagious and is spread by direct skin contact or by airborne transmission and can result in amputation or death. In addition, MRSA is very difficult to treat because it is resistant to many antibiotics. For example, β-lactamβ-lactam antibiotics, such as penicillin, function by binding to and inactivating bacterial penicillin-binding proteins (PBPs), which synthesize the bacterial cell wall. However, MRSA expresses an alternative type of PBP, called PBP2a encoded by the mecA gene. β-lactamβ-lactam antibiotics only weakly bind PBP2a, and thus cell wall synthesis can continue in their presence. Moreover, in a system somewhat analogous to the regulation of the lac operon, mecA is induced by the presence of β-lactamβ-lactam antibiotics and repressed in their absence. This “on-demand” expression of mecA means that when the infection is treated with antibiotics, the cells ramp up their resistance.

1. Chen et al. [Antimicrob. Agents Chemother. (2014) 58(2):1047–1054] studied several strains of MRSA isolated in Taiwan and found that some single point mutations in the mecA promoter were linked to increased antibiotic resistance while other point mutations were linked to decreased antibiotic resistance. Why might mecA promoter mutations have these opposing effects?