Cell splitting in Staphylococcus aureus is controlled by an adaptor protein facilitating degradation of a peptidoglycan hydrolase.

This study used a genome-wide screen, sequencing of suppressor mutants, immunoblotting, and in vivo protein-protein interaction assays to uncover the role of the uncharacterized protein CxaR in controlling Staphylococcus aureus cell splitting. The researchers found that CxaR acts as an adaptor protein, facilitating the degradation of the peptidoglycan hydrolase Sle1 by the conserved ClpXP protease complex. This tight regulation of Sle1 levels is crucial for maintaining the balance between peptidoglycan biosynthesis and hydrolysis, which is disrupted by β-lactam antibiotics, leading to their bactericidal effects. The findings provide insights into the mechanisms underlying cell division in S. aureus and have implications for understanding the action of β-lactam antibiotics.