{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhu W"],"funding":["Project of MOE Key Laboratory of Geriatric Diseases and Immunology, Soochow University","MOST | National Natural Science Foundation of China (NSFC)","MOST | National Natural Science Foundation of China"],"pagination":["e0077224"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11656735"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["9(12)"],"pubmed_abstract":["Enzyme-IIA (EIIA<sup>Glc</sup>, Crr) of the phosphotransferase system (PTS) connects the uptake of glucose-family sugars to the cAMP-Crp regulatory cascade; phosphorylated EIIA<sup>Glc</sup> enhances cAMP-Crp activity, which then contributes to the antibiotic-mediated accumulation of reactive oxygen species (ROS) and cell death. Defects in PTS cause antibiotic and disinfectant tolerance. We report that mannitol, a carbon source whose uptake does not use EIIA<sup>Glc</sup>, reduces antibiotic-mediated killing of <i>Escherichia coli</i> without affecting antibiotic minimal inhibitory concentration. Thus, mannitol promotes antibiotic tolerance. The tolerance pathway was defined by the loss of ciprofloxacin lethality from the deletion of <i>ptsI</i> (first gene in PTS), <i>mtlA</i> (mannitol-s"],"journal":["mSphere"],"pubmed_title":["Antibiotic tolerance due to restriction of cAMP-Crp regulation by mannitol, a non-glucose-family PTS carbon source."],"pmcid":["PMC11656735"],"funding_grant_id":["82172316","KJS2401"],"pubmed_authors":["Liao Y","Drlica K","Wang B","Chen M","Guo W","Wang D","Su J","Xue Y","Zhao X","Hong Y","Zhang X","Niu J","Nong Y","Zhu W"],"additional_accession":[]},"is_claimable":false,"name":"Antibiotic tolerance due to restriction of cAMP-Crp regulation by mannitol, a non-glucose-family PTS carbon source.","description":"Enzyme-IIA (EIIA<sup>Glc</sup>, Crr) of the phosphotransferase system (PTS) connects the uptake of glucose-family sugars to the cAMP-Crp regulatory cascade; phosphorylated EIIA<sup>Glc</sup> enhances cAMP-Crp activity, which then contributes to the antibiotic-mediated accumulation of reactive oxygen species (ROS) and cell death. Defects in PTS cause antibiotic and disinfectant tolerance. We report that mannitol, a carbon source whose uptake does not use EIIA<sup>Glc</sup>, reduces antibiotic-mediated killing of <i>Escherichia coli</i> without affecting antibiotic minimal inhibitory concentration. Thus, mannitol promotes antibiotic tolerance. The tolerance pathway was defined by the loss of ciprofloxacin lethality from the deletion of <i>ptsI</i> (first gene in PTS), <i>mtlA</i> (mannitol-s","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Dec","modification":"2025-04-18T14:40:30.653Z","creation":"2025-04-07T00:57:03.99Z"},"accession":"S-EPMC11656735","cross_references":{"pubmed":["39565127"],"doi":["10.1128/msphere.00772-24"]}}