In 2013, there was an outbreak of methicillin-resistant Staphylococcusaureus (MRSA) at an NFL training facility. One player suffereda career-ending infection to his foot and sued the team owners for $20 million for unsanitary conditions that contributed to the bacterialinfection. A settlement with undisclosed terms was reached in2017. MRSA is highly contagious and is spread by direct skin contactor by airborne transmission and can result in amputation or death.In addition, MRSA is very difficult to treat because it is resistant tomany antibiotics. For example, b -lactam antibiotics, such as penicillin,function by binding to and inactivating bacterial penicillin-bindingproteins (PBPs), which synthesize the bacterial cell wall. However,MRSA expresses an alternative type of PBP, called PBP2a encodedby the mecA gene. b -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 lacoperon, mecA is induced by the presence of b -lactam antibiotics andrepressed in their absence. This “on-demand” expression of mecA means that when the infection is treated with antibiotics, the cellsramp up their resistance. Question:Chen et al. [Antimicrob. Agents Chemother. (2014) 58(2):1047–1054] studied several strains of MRSA isolated in Taiwanand found that some single point mutations in the mecA promoterwere linked to increased antibiotic resistance while other pointmutations were linked to decreased antibiotic resistance. Whymight mecA promoter mutations have these opposing effects?
In 2013, there was an outbreak of methicillin-resistant Staphylococcusaureus (MRSA) at an NFL training facility. One player suffereda career-ending infection to his foot and sued the team owners for $20 million for unsanitary conditions that contributed to the bacterialinfection. A settlement with undisclosed terms was reached in2017. MRSA is highly contagious and is spread by direct skin contactor by airborne transmission and can result in amputation or death.In addition, MRSA is very difficult to treat because it is resistant tomany antibiotics. For example, b -lactam antibiotics, such as penicillin,function by binding to and inactivating bacterial penicillin-bindingproteins (PBPs), which synthesize the bacterial cell wall. However,MRSA expresses an alternative type of PBP, called PBP2a encodedby the mecA gene. b -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 lacoperon, mecA is induced by the presence of b -lactam antibiotics andrepressed in their absence. This “on-demand” expression of mecA means that when the infection is treated with antibiotics, the cellsramp up their resistance.
Question: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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