{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"omics_type":["Unknown"],"submitter":["Hurst MN"],"funding":["NIDDK NIH HHS","NIAID NIH HHS"],"pubmed_abstract":["The modification of lipopolysaccharide (LPS) in <i>Escherichia coli</i> and <i>Salmonella spp</i> . is primarily controlled by the two-component system PmrAB. LPS modification allows bacteria to avoid killing by positively charged antibiotics like polymyxin B. We previously demonstrated that in uropathogenic <i>E. coli</i> (UPEC), the sensor histidine kinase PmrB also activates a non-cognate transcription factor, QseB, and this activation somehow augments polymyxin B tolerance in UPEC. Here, we demonstrate - for the first time - that in the absence of the canonical LPS transcriptional regulator, PmrA, QseB can direct some modifications on the LPS. In agreement with this observation, transcriptional profiling analyses demonstrate regulatory overlaps between PmrA and QseB in terms of regulat"],"journal":["bioRxiv : the preprint server for biology"],"pagination":["2023.01.10.523522"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC9882033"],"repository":["biostudies-literature"],"pubmed_title":["The QseB response regulator imparts tolerance to positively charged antibiotics by controlling metabolism and minor changes to LPS."],"pmcid":["PMC9882033"],"funding_grant_id":["F31 AI143244","P50 DK064540","R01 AI129940","R01 AI107052","P20 DK123967","R01 AI138576","R01 AI048689","R01 AI150098"],"pubmed_authors":["Beebout CJ","Reasoner SA","Hurst MN","Guckes KR","Purcell A","Bermudez TA","Hollingsworth A","Williams D","Hadjifrangiskou M","Trent MS"],"additional_accession":[]},"is_claimable":false,"name":"The QseB response regulator imparts tolerance to positively charged antibiotics by controlling metabolism and minor changes to LPS.","description":"The modification of lipopolysaccharide (LPS) in <i>Escherichia coli</i> and <i>Salmonella spp</i> . is primarily controlled by the two-component system PmrAB. LPS modification allows bacteria to avoid killing by positively charged antibiotics like polymyxin B. We previously demonstrated that in uropathogenic <i>E. coli</i> (UPEC), the sensor histidine kinase PmrB also activates a non-cognate transcription factor, QseB, and this activation somehow augments polymyxin B tolerance in UPEC. Here, we demonstrate - for the first time - that in the absence of the canonical LPS transcriptional regulator, PmrA, QseB can direct some modifications on the LPS. In agreement with this observation, transcriptional profiling analyses demonstrate regulatory overlaps between PmrA and QseB in terms of regulat","dates":{"release":"2023-01-01T00:00:00Z","publication":"2023 Jan","modification":"2025-04-04T20:52:28.379Z","creation":"2024-11-20T20:32:10.495Z"},"accession":"S-EPMC9882033","cross_references":{"pubmed":["36711705"],"doi":["10.1101/2023.01.10.523522"]}}