{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Liu JL"],"funding":["Canadian Institutes of Health Research"],"pagination":["e1002553"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3305355"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["8(3)"],"pubmed_abstract":["Mammalian bile acids (BAs) are oxidized metabolites of cholesterol whose amphiphilic properties serve in lipid and cholesterol uptake. BAs also act as hormone-like substances that regulate metabolism. The Caenorhabditis elegans clk-1 mutants sustain elevated mitochondrial oxidative stress and display a slow defecation phenotype that is sensitive to the level of dietary cholesterol. We found that: 1) The defecation phenotype of clk-1 mutants is suppressed by mutations in tat-2 identified in a previous unbiased screen for suppressors of clk-1. TAT-2 is homologous to ATP8B1, a flippase required for normal BA secretion in mammals. 2) The phenotype is suppressed by cholestyramine, a resin that binds BAs. 3) The phenotype is suppressed by the knock-down of C. elegans homologues of BA-biosyntheti"],"journal":["PLoS genetics"],"pubmed_title":["Mitochondrial oxidative stress alters a pathway in Caenorhabditis elegans strongly resembling that of bile acid biosynthesis and secretion in vertebrates."],"pmcid":["PMC3305355"],"funding_grant_id":["MOP-89761"],"pubmed_authors":["Desjardins D","Hekimi S","Liu JL","Agellon LB","Branicky R"],"additional_accession":[]},"is_claimable":false,"name":"Mitochondrial oxidative stress alters a pathway in Caenorhabditis elegans strongly resembling that of bile acid biosynthesis and secretion in vertebrates.","description":"Mammalian bile acids (BAs) are oxidized metabolites of cholesterol whose amphiphilic properties serve in lipid and cholesterol uptake. BAs also act as hormone-like substances that regulate metabolism. The Caenorhabditis elegans clk-1 mutants sustain elevated mitochondrial oxidative stress and display a slow defecation phenotype that is sensitive to the level of dietary cholesterol. We found that: 1) The defecation phenotype of clk-1 mutants is suppressed by mutations in tat-2 identified in a previous unbiased screen for suppressors of clk-1. TAT-2 is homologous to ATP8B1, a flippase required for normal BA secretion in mammals. 2) The phenotype is suppressed by cholestyramine, a resin that binds BAs. 3) The phenotype is suppressed by the knock-down of C. elegans homologues of BA-biosyntheti","dates":{"release":"2012-01-01T00:00:00Z","publication":"2012","modification":"2026-04-30T09:44:03.862Z","creation":"2019-03-27T00:51:12Z"},"accession":"S-EPMC3305355","cross_references":{"pubmed":["22438816"],"doi":["10.1371/journal.pgen.1002553"]}}