<HashMap><database>biostudies-literature</database><scores><citationCount>0</citationCount><reanalysisCount>0</reanalysisCount><viewCount>53</viewCount><searchCount>0</searchCount></scores><additional><submitter>Shakoury-Elizeh M</submitter><funding>NIDDK NIH HHS</funding><funding>NINDS NIH HHS</funding><funding>NIGMS NIH HHS</funding><pagination>14823-33</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC2863190</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>285(19)</volume><pubmed_abstract>Iron is an essential cofactor for enzymes involved in numerous cellular processes, yet little is known about the impact of iron deficiency on cellular metabolism or iron proteins. Previous studies have focused on changes in transcript and proteins levels in iron-deficient cells, yet these changes may not reflect changes in transport activity or flux through a metabolic pathway. We analyzed the metabolomes and transcriptomes of yeast grown in iron-rich and iron-poor media to determine which biosynthetic processes are altered when iron availability falls. Iron deficiency led to changes in glucose metabolism, amino acid biosynthesis, and lipid biosynthesis that were due to deficiencies in specific iron-dependent enzymes. Iron-sulfur proteins exhibited loss of iron cofactors, yet amino acid synthesis was maintained. Ergosterol and sphingolipid biosynthetic pathways had blocks at points where heme and diiron enzymes function, whereas Ole1, the essential fatty acid desaturase, was resistant to iron depletion. Iron-deficient cells exhibited depletion of most iron enzyme activities, but loss of activity during iron deficiency did not consistently disrupt metabolism. Amino acid homeostasis was robust, but iron deficiency impaired lipid synthesis, altering the properties and functions of cellular membranes.</pubmed_abstract><journal>The Journal of biological chemistry</journal><pubmed_title>Metabolic response to iron deficiency in Saccharomyces cerevisiae.</pubmed_title><pmcid>PMC2863190</pmcid><funding_grant_id>GM62104</funding_grant_id><funding_grant_id>P30 DK072437</funding_grant_id><funding_grant_id>R01 NS047717</funding_grant_id><funding_grant_id>NS47717</funding_grant_id><funding_grant_id>R01 GM062104</funding_grant_id><pubmed_authors>Berger A</pubmed_authors><pubmed_authors>Prinz WA</pubmed_authors><pubmed_authors>Cox J</pubmed_authors><pubmed_authors>Bard M</pubmed_authors><pubmed_authors>Protchenko O</pubmed_authors><pubmed_authors>Gable K</pubmed_authors><pubmed_authors>Dunn TM</pubmed_authors><pubmed_authors>Philpott CC</pubmed_authors><pubmed_authors>Shakoury-Elizeh M</pubmed_authors><view_count>53</view_count></additional><is_claimable>false</is_claimable><name>Metabolic response to iron deficiency in Saccharomyces cerevisiae.</name><description>Iron is an essential cofactor for enzymes involved in numerous cellular processes, yet little is known about the impact of iron deficiency on cellular metabolism or iron proteins. Previous studies have focused on changes in transcript and proteins levels in iron-deficient cells, yet these changes may not reflect changes in transport activity or flux through a metabolic pathway. We analyzed the metabolomes and transcriptomes of yeast grown in iron-rich and iron-poor media to determine which biosynthetic processes are altered when iron availability falls. Iron deficiency led to changes in glucose metabolism, amino acid biosynthesis, and lipid biosynthesis that were due to deficiencies in specific iron-dependent enzymes. Iron-sulfur proteins exhibited loss of iron cofactors, yet amino acid synthesis was maintained. Ergosterol and sphingolipid biosynthetic pathways had blocks at points where heme and diiron enzymes function, whereas Ole1, the essential fatty acid desaturase, was resistant to iron depletion. Iron-deficient cells exhibited depletion of most iron enzyme activities, but loss of activity during iron deficiency did not consistently disrupt metabolism. Amino acid homeostasis was robust, but iron deficiency impaired lipid synthesis, altering the properties and functions of cellular membranes.</description><dates><release>2010-01-01T00:00:00Z</release><publication>2010 May</publication><modification>2021-02-20T19:08:45Z</modification><creation>2019-03-27T00:30:30Z</creation></dates><accession>S-EPMC2863190</accession><cross_references><pubmed>20231268</pubmed><doi>10.1074/jbc.m109.091710</doi><doi>10.1074/jbc.M109.091710</doi></cross_references></HashMap>