The Sle1 Cell Wall Amidase Is Essential for β-Lactam Resistance in Community-Acquired Methicillin-Resistant Staphylococcus aureus USA300.

ABSTRACT: Most clinically relevant methicillin-resistant Staphylococcus aureus (MRSA) strains have become resistant to β-lactams antibiotics through horizontal acquisition of the mecA gene encoding PBP2a, a peptidoglycan transpeptidase with low affinity for β-lactams. The level of resistance conferred by mecA is, however, strain dependent, and the mechanisms underlying this phenomenon remain poorly understood. We show here that β-lactam resistance correlates to expression of the Sle1 cell wall amidase in the fast-spreading and highly virulent community-acquired MRSA USA300 clone. Sle1 is a substrate of the ClpXP protease, and while the high Sle1 levels in cells lacking ClpXP activity confer β-lactam hyper-resistance, USA300 cells lacking Sle1 are as susceptible to β-lactams as c

SUBMITTER: Thalso-Madsen I 

PROVIDER: S-EPMC7187620 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature