{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Gyger J"],"funding":["Swiss National Science Foundation","Howard Hughes Medical Institute","NIAID NIH HHS","HHS | NIH | National Institute of Allergy and Infectious Diseases","Howard Hughes Medical Institute (HHMI)"],"pagination":["e0141924"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11253642"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["15(7)"],"pubmed_abstract":["<i>Pseudomonas aeruginosa</i> encodes the beta-lactamase AmpC, which promotes resistance to beta-lactam antibiotics. Expression of <i>ampC</i> is induced by anhydro-muropeptides (AMPs) released from the peptidoglycan (PG) cell wall upon beta-lactam treatment. AmpC can also be induced via genetic inactivation of PG biogenesis factors such as the endopeptidase DacB that cleaves PG crosslinks. Mutants in <i>dacB</i> occur in beta-lactam-resistant clinical isolates of <i>P. aeruginosa</i>, but it has remained unclear why DacB inactivation promotes <i>ampC</i> induction. Similarly, the inactivation of lytic transglycosylase (LT) enzymes such as SltB1 that cut PG glycans has also been associated with <i>ampC</i> induction and beta-lactam resistance. Given that LT enzymes are capable of producing"],"journal":["mBio"],"pubmed_title":["A potential space-making role in cell wall biogenesis for SltB1and DacB revealed by a beta-lactamase induction phenotype in <i>Pseudomonas aeruginosa</i>."],"pmcid":["PMC11253642"],"funding_grant_id":["R01 AI083365","U19 AI158028","162073"],"pubmed_authors":["Bernhardt TG","Gyger J","Cava F","Torrens G","Fumeaux C"],"additional_accession":[]},"is_claimable":false,"name":"A potential space-making role in cell wall biogenesis for SltB1and DacB revealed by a beta-lactamase induction phenotype in <i>Pseudomonas aeruginosa</i>.","description":"<i>Pseudomonas aeruginosa</i> encodes the beta-lactamase AmpC, which promotes resistance to beta-lactam antibiotics. Expression of <i>ampC</i> is induced by anhydro-muropeptides (AMPs) released from the peptidoglycan (PG) cell wall upon beta-lactam treatment. AmpC can also be induced via genetic inactivation of PG biogenesis factors such as the endopeptidase DacB that cleaves PG crosslinks. Mutants in <i>dacB</i> occur in beta-lactam-resistant clinical isolates of <i>P. aeruginosa</i>, but it has remained unclear why DacB inactivation promotes <i>ampC</i> induction. Similarly, the inactivation of lytic transglycosylase (LT) enzymes such as SltB1 that cut PG glycans has also been associated with <i>ampC</i> induction and beta-lactam resistance. Given that LT enzymes are capable of producing","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2025-04-04T15:01:37.164Z","creation":"2025-04-04T15:01:37.164Z"},"accession":"S-EPMC11253642","cross_references":{"pubmed":["38920394"],"doi":["10.1128/mbio.01419-24"]}}