<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Banerjee R</submitter><funding>HHS | National Institutes of Health</funding><funding>NIGMS NIH HHS</funding><funding>Robert Turrel Endowment</funding><funding>National Science Foundation</funding><pagination>e00351-20</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC7157518</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>11(2)</volume><pubmed_abstract>Pathogenicity islands and plasmids bear genes for pathogenesis of various &lt;i>Escherichia coli&lt;/i> pathotypes. Although there is a basic understanding of the contribution of these virulence factors to disease, less is known about variation in regulatory networks in determining disease phenotypes. Here, we dissected a regulatory network directed by the conserved iron homeostasis regulator, ferric uptake regulator (Fur), in uropathogenic &lt;i>E. coli&lt;/i> (UPEC) strain CFT073. Comparing anaerobic genome-scale Fur DNA binding with Fur-dependent transcript expression and protein levels of the uropathogen to that of commensal &lt;i>E. coli&lt;/i> K-12 strain MG1655 showed that the Fur regulon of the core genome is conserved but also includes genes within the pathogenicity/genetic islands. Unexpectedly, r</pubmed_abstract><journal>mBio</journal><pubmed_title>Tailoring a Global Iron Regulon to a Uropathogen.</pubmed_title><pmcid>PMC7157518</pmcid><funding_grant_id>R01 GM115894</funding_grant_id><funding_grant_id>1818303</funding_grant_id><funding_grant_id>GM108538</funding_grant_id><funding_grant_id>GM115894</funding_grant_id><funding_grant_id>P41 GM108538</funding_grant_id><pubmed_authors>Perna NT</pubmed_authors><pubmed_authors>Kiley PJ</pubmed_authors><pubmed_authors>Banerjee R</pubmed_authors><pubmed_authors>Glasner JD</pubmed_authors><pubmed_authors>Welch RA</pubmed_authors><pubmed_authors>Schwartz KJ</pubmed_authors><pubmed_authors>Weisenhorn E</pubmed_authors><pubmed_authors>Myers KS</pubmed_authors><pubmed_authors>Coon JJ</pubmed_authors></additional><is_claimable>false</is_claimable><name>Tailoring a Global Iron Regulon to a Uropathogen.</name><description>Pathogenicity islands and plasmids bear genes for pathogenesis of various &lt;i>Escherichia coli&lt;/i> pathotypes. Although there is a basic understanding of the contribution of these virulence factors to disease, less is known about variation in regulatory networks in determining disease phenotypes. Here, we dissected a regulatory network directed by the conserved iron homeostasis regulator, ferric uptake regulator (Fur), in uropathogenic &lt;i>E. coli&lt;/i> (UPEC) strain CFT073. Comparing anaerobic genome-scale Fur DNA binding with Fur-dependent transcript expression and protein levels of the uropathogen to that of commensal &lt;i>E. coli&lt;/i> K-12 strain MG1655 showed that the Fur regulon of the core genome is conserved but also includes genes within the pathogenicity/genetic islands. Unexpectedly, r</description><dates><release>2020-01-01T00:00:00Z</release><publication>2020 Mar</publication><modification>2026-06-07T07:58:54.421Z</modification><creation>2025-06-01T03:54:25.392Z</creation></dates><accession>S-EPMC7157518</accession><cross_references><pubmed>32209682</pubmed><doi>10.1128/mBio.00351-20</doi></cross_references></HashMap>