Staphylococcus aureus lacking a functional MntABC manganese import system has increased resistance to copper

Area of Science:

• Microbiology
• Molecular Biology
• Biochemistry

Background:

• Staphylococcus aureus USA300 possesses copper homeostasis mechanisms (copBL and copAZ) to prevent copper intoxication.
• Copper accumulation can be detrimental to bacterial cells, impacting essential enzyme functions.

Purpose of the Study:

• To investigate the role of the mntABC operon in copper resistance in S. aureus USA300.
• To elucidate the relationship between manganese import and copper tolerance.

Main Methods:

• Construction and analysis of a copper-sensitive mutant (ΔcopAZ ΔcopBL).
• Screening of a transposon mutant library to identify genes conferring copper resistance.
• Genetic manipulation including gene deletions and over-expression.

Main Results:

• Mutations in the mntA gene of the mntABC operon conferred copper resistance by reducing intracellular copper accumulation.
• Manganese supplementation enhanced growth in copper, dependent on the repressor MntR.
• Defective MntABC protected iron-sulfur enzymes from copper-induced inactivation.

Conclusions:

• The MntABC manganese import system plays a crucial role in cellular copper accumulation in S. aureus.
• Impaired MntABC function confers resistance to copper toxicity by limiting intracellular copper levels and protecting essential enzymes.