{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Yigit K"],"funding":["HHS | NIH | National Institute of General Medical Sciences","HHS | NIH | National Institute of General Medical Sciences (NIGMS)","NIGMS NIH HHS"],"pagination":["e0023724"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC11270865"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["206(7)"],"pubmed_abstract":["Responding to changes in oxygen levels is critical for aerobic microbes. In <i>Caulobacter crescentus</i>, low oxygen is sensed by the FixL-FixJ two-component system which induces multiple genes, including those involved in heme biosynthesis, to accommodate microaerobic conditions. The FixLJ inhibitor FixT is also induced under low oxygen conditions and is degraded by the Lon protease when the oxygen levels are sufficient, which together provides negative feedback proposed to adjust FixLJ signaling thresholds during changing conditions. Here, we address whether degradation of FixT by the Lon protease contributes to phenotypic defects associated with loss of Lon. We find that ∆<i>lon</i> strains are deficient in FixLJ-dependent heme biosynthesis, consistent with elevated FixT levels as dele"],"journal":["Journal of bacteriology"],"pubmed_title":["Proteolytic control of FixT by the Lon protease impacts FixLJ signaling in <i>Caulobacter crescentus</i>."],"pmcid":["PMC11270865"],"funding_grant_id":["R35GM130320, T32GM139789","R35 GM130320","T32 GM139789","R35GM130320"],"pubmed_authors":["Yigit K","Chien P"],"additional_accession":[]},"is_claimable":false,"name":"Proteolytic control of FixT by the Lon protease impacts FixLJ signaling in <i>Caulobacter crescentus</i>.","description":"Responding to changes in oxygen levels is critical for aerobic microbes. In <i>Caulobacter crescentus</i>, low oxygen is sensed by the FixL-FixJ two-component system which induces multiple genes, including those involved in heme biosynthesis, to accommodate microaerobic conditions. The FixLJ inhibitor FixT is also induced under low oxygen conditions and is degraded by the Lon protease when the oxygen levels are sufficient, which together provides negative feedback proposed to adjust FixLJ signaling thresholds during changing conditions. Here, we address whether degradation of FixT by the Lon protease contributes to phenotypic defects associated with loss of Lon. We find that ∆<i>lon</i> strains are deficient in FixLJ-dependent heme biosynthesis, consistent with elevated FixT levels as dele","dates":{"release":"2024-01-01T00:00:00Z","publication":"2024 Jul","modification":"2025-04-03T23:19:04.341Z","creation":"2025-04-03T23:19:04.341Z"},"accession":"S-EPMC11270865","cross_references":{"pubmed":["38940598"],"doi":["10.1128/jb.00237-24"]}}