<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><submitter>Rios-Delgado G</submitter><funding>NIEHS NIH HHS</funding><funding>NIAID NIH HHS</funding><pubmed_abstract>&lt;i>Staphylococcus aureus&lt;/i> has evolved mechanisms to cope with low iron (Fe) availability in host tissues. &lt;i>S. aureus&lt;/i> uses the ferric uptake transcriptional regulator (Fur) to sense titers of cytosolic Fe. Upon Fe depletion, apo-Fur relieves transcriptional repression of genes utilized for Fe uptake. We demonstrate that an &lt;i>S. aureus&lt;/i> Δ&lt;i>fur&lt;/i> mutant has decreased expression of &lt;i>acnA&lt;/i>, which codes for the Fe-dependent enzyme aconitase. Decreased &lt;i>acnA&lt;/i> expression prevented the Δ&lt;i>fur&lt;/i> mutant from growing with amino acids as sole carbon and energy sources. Suppressor analysis determined that a mutation in &lt;i>isrR&lt;/i>, which produces a regulatory RNA, permitted growth by decreasing &lt;i>isrR&lt;/i> transcription. The decreased AcnA activity of the Δ&lt;i>fur&lt;/i> mutant </pubmed_abstract><journal>bioRxiv : the preprint server for biology</journal><pagination>2024.07.03.601953</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC11245030</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>The &amp;lt;i&amp;gt;Staphylococcus aureus&amp;lt;/i&amp;gt; small non-coding RNA IsrR regulates TCA cycle activity and virulence.</pubmed_title><pmcid>PMC11245030</pmcid><funding_grant_id>R21 AI156251</funding_grant_id><funding_grant_id>R21 AI153646</funding_grant_id><funding_grant_id>T32 ES007028</funding_grant_id><funding_grant_id>F31 AI172352</funding_grant_id><pubmed_authors>Lalaouna D</pubmed_authors><pubmed_authors>Zelzion E</pubmed_authors><pubmed_authors>Rios-Delgado G</pubmed_authors><pubmed_authors>Briaud P</pubmed_authors><pubmed_authors>Norambuena J</pubmed_authors><pubmed_authors>McReynolds AKG</pubmed_authors><pubmed_authors>Kim J</pubmed_authors><pubmed_authors>Bose JL</pubmed_authors><pubmed_authors>Zheng V</pubmed_authors><pubmed_authors>Parker D</pubmed_authors><pubmed_authors>Pagella EA</pubmed_authors><pubmed_authors>Racine H</pubmed_authors><pubmed_authors>Boyd JM</pubmed_authors><pubmed_authors>Carroll R</pubmed_authors><pubmed_authors>Munneke MJ</pubmed_authors><pubmed_authors>Skaar E</pubmed_authors></additional><is_claimable>false</is_claimable><name>The &amp;lt;i&amp;gt;Staphylococcus aureus&amp;lt;/i&amp;gt; small non-coding RNA IsrR regulates TCA cycle activity and virulence.</name><description>&lt;i>Staphylococcus aureus&lt;/i> has evolved mechanisms to cope with low iron (Fe) availability in host tissues. &lt;i>S. aureus&lt;/i> uses the ferric uptake transcriptional regulator (Fur) to sense titers of cytosolic Fe. Upon Fe depletion, apo-Fur relieves transcriptional repression of genes utilized for Fe uptake. We demonstrate that an &lt;i>S. aureus&lt;/i> Δ&lt;i>fur&lt;/i> mutant has decreased expression of &lt;i>acnA&lt;/i>, which codes for the Fe-dependent enzyme aconitase. Decreased &lt;i>acnA&lt;/i> expression prevented the Δ&lt;i>fur&lt;/i> mutant from growing with amino acids as sole carbon and energy sources. Suppressor analysis determined that a mutation in &lt;i>isrR&lt;/i>, which produces a regulatory RNA, permitted growth by decreasing &lt;i>isrR&lt;/i> transcription. The decreased AcnA activity of the Δ&lt;i>fur&lt;/i> mutant </description><dates><release>2024-01-01T00:00:00Z</release><publication>2024 Jul</publication><modification>2025-04-04T01:18:52.549Z</modification><creation>2025-04-04T01:18:52.549Z</creation></dates><accession>S-EPMC11245030</accession><cross_references><pubmed>39005296</pubmed><doi>10.1101/2024.07.03.601953</doi></cross_references></HashMap>