Zinc starvation uncovers bacterial host-specific proteases that shape NDM adaptability in <i>Acinetobacter baumannii</i>.

ABSTRACT: Metallo-β-lactamases, particularly New Delhi metallo-β-lactamase (NDM), threaten antibiotic therapy by disseminating across diverse bacteria. The rise of NDM-producing carbapenem-resistant Acinetobacter baumannii (Ab) highlights the risk of global spread of this pathogen. NDM-mediated resistance depends on periplasmic proteostasis, which regulates the levels of folded, metalated, and active proteins. In Escherichia coli, zinc limitation-common at infection sites-causes loss of the essential metal cofactors in NDM, leading to protein degradation via a specific periplasmic quality control system. Our study reveals that the mechanisms regulating NDM-1 stability under zinc starvation are highly host-dependent. Notably, we identify the proteases DegP and CtpA as responsible

SUBMITTER: Parodi C 

PROVIDER: S-EPMC12802154 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature