A D-alanine aminotransferase S₁₈₀F substitution confers resistance to β-chloro-D-alanine in <i>Staphylococcus aureus</i> via antibiotic inactivation.

ABSTRACT: Alanine transport and metabolism impact MRSA pathophysiology by dictating the availability of d-alanine for cell wall synthesis, the target of β-lactam antibiotics. Furthermore cycA-dependent alanine transport controls MRSA β-lactam susceptibility in chemically defined medium (CDM) in a glucose-dependent manner. Here we report that S. aureus was auxotrophic for l-alanine in CDM, and that this growth defect was rescued by glucose (or compensatory mutations), but only when the alanine racemase (alr1) and d-alanine aminotransferase (dat) genes were functional. No role was observed for the alanine dehydrogenase 1 (ald1) and ald2 genes. As previously reported, alr1 and, to a lesser extent, cycA mutations increased susceptibility to d-cyclo

SUBMITTER: Roy R 

PROVIDER: S-EPMC12393368 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature