Methicillin-resistant <i>Staphylococcus aureus</i> (MRSA) has been difficult to treat because of its resistance to multiple antibiotics. One way this is being combated is through the development of antibiotic adjuvants. These adjuvants have no activity on their own, but when combined with an antibiotic, the cotreatment results in bacteria becoming sensitive to the antibiotic again. Our lab has identified small molecule adjuvants that potentiate beta-lactam antibiotics in MRSA. We are now exploring how these adjuvants work at the molecular level. Based on previous results, we are first focusing on a master regulator called eukaryotic-like serine-threonine kinase 1 (Stk1). This protein contributes to MRSA’s virulence by regulating biofilm formation and antibiotic resistance. The CRISPR-Cas9 system has recently been used for efficient genome editing in this organism that historically has been difficult to genetically manipulate. The research that will be presented uses CRISPR-Cas9 to create novel knockout mutants of the stk1 gene in MRSA strains that are clinically relevant. These mutants will then be used in our efforts to find out more about the strain-specific functions of Stk1. Other strain-specific differences will also be reported.

Using CRISPR-Cas9 to delete stk1 in MRSA

ACS Spring 2022

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