Staphylococcus aureus is capable of causing numerous types of infections in humans that range from mild to serious. Indeed, S. aureus can cause minor skin infections such as boils or it can cause more serious infections that result in clinical manifestations such as endocarditis, osteomyelitis, arthritis, septicemia, and toxic shock syndrome, among others, as well as infections of surgical wounds. What is more, S. aureus is known as one of the so-called superbugs, because of the pathogenic nature of the bacterium combined with the fact that it frequently acquires resistance to many currently used antibiotics. Methicillin resistant S. aureus, or MRSA, is one of the most notorious pathogens in the hospital environment and the spread of community acquired MRSA is now becoming prevalent.
The Heinrichs lab investigates the molecular basis of MRSA infections, with a special focus on the mechanisms MRSA uses to acquire growth promoting nutrients. Using a wide range of molecular and biochemical tools, the lab aims to answer the following questions:
How does MRSA scavenge nutrients during infection?
how does MRSA regulate nutrient source preference?
how does mrsa liberate nutrients from the host?
How does inhibiting nutrient acquisition pathways affect the outcome of MRSA infection?
Goncheva MI, et al. 2019. Stress-induced inactivation of the Staphylococcus aureus purine biosynthesis repressor leads to hypervirulence. Nature Communications 10(1):775.
Kaiser JC, King AN, Grigg JC, Sheldon JR, Edgell DR, Murphy MEP, Brinsmade SR, Heinrichs DE. 2018. Repression of branched-chain amino acid synthesis in Staphylococcus aureus is mediated by isoleucine via CodY, and by a leucine-rich attenuator peptide. PLOS Genetics Jan 22; 14(1):e1007159.
Laakso HA, Marolda CL, Pinter TB, Stillman MJ and Heinrichs DE. 2016. A heme-responsive regulator controls synthesis of staphyloferrin B in Staphylococcus aureus. Journal of Biological Chemistry 291: 29-40.