S. aureus is a gram positive cocci, this bacteria asymptomatically colonizes 1/3 of individuals, and has the ability to infect nearly every body site. Infection can lead to conditions such as endocarditis, pneumonia, sepsis, toxic shock syndrome, osteomyelitis, and soft tissue infections. The public health threat of S. aureus is compounded by the rise of antibiotic resistance, most notably methicillin-resistant S. aureus (MRSA). 

The ability to readily sense environmental changes and accordingly shift cellular physiology opens niches for S. aureus within different tissues and confers intrinsic resistance to antibiotic treatments, contributing to S. aureus’s virulence, persistence, and success as a pathogen. 

The eukaryotic like PASTA Kinase known as Stk1 has been shown to be a cirtical player in β-lactam resistance in S. aureus. Additionally, stk1 is highly conserved amongst Gram Positives, Myobacteria. This kinase can be considered a master regulator with controls over processes like carbon metabolism, biofilm, and most pertaining to our lab, cell wall stress. 

There are many stress mechanisms in S.aureus that have evolved to make the bacteria more successful in its virulence. However, the mechanism of how S.aureus responds to antibiotic stress is still unknown. This is the main focus of the Grunenwald Lab.