<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE314nnn/GSE314968/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Streptococcus mutans</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE314968</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>An XRE-Type Regulator in Streptococcus mutans Plays an Important Role in brpA Expression and Oxidative Stress Tolerance Response</name><description>Locus SMU.405 encodes a xenobiotic response element (XRE) family transcriptional regulator. This study used a functional genomics approach to explore the role of a XRE-type regulator (SMU.405c) in S. mutans physiology including the expression of biofilm regulatory protein BrpA. Results showed that deletional mutation of xre significantly reduced the ability of the deficient mutant to grow in the presence of methyl viologen, a commonly used oxidative stressor (P&lt;0.001). When challenged in a hydrogen peroxide killing assay, the survival rate of the ∆xre mutant was >2-log less than the parent strain after 60 minutes (P&lt;0.001). Luciferase reporter fusion assays showed that xre deficiency had no significant effect on luciferase expression when it was under the control of the intact brpA promoter, but the reporter activity increased by >6-fold (P&lt;0.001) when the reporter gene was fused to a brpA promoter derivative with deletion of a putative XRE-binding box. EMSA assay showed that recombinant XRE interacted with the brpA promoter, resulting in electrophoretic shift of the promoter probes. In vitro transcription assay also showed that inclusion of XRE caused transcription to fall-off, significantly reducing full-length brpA transcripts. RNA-seq analysis revealed that deficiency of XRE led to altered expression of >102 genes by >2-fold (P&lt;0.05), including 28 with increased expression and 74 with decreased expression. Among the down regulated were genes for DNA repair and oxidative stress tolerance response. These results suggest that XRE (SMU.405c) in S. mutans plays an important role in brpA expression and oxidative stress tolerance response.</description><dates><publication>2026/06/10</publication></dates><accession>GSE314968</accession><cross_references><GSM>GSM9417239</GSM><GSM>GSM9417244</GSM><GSM>GSM9417240</GSM><GSM>GSM9417241</GSM><GSM>GSM9417242</GSM><GSM>GSM9417243</GSM><GPL>36456</GPL><GSE>314968</GSE><taxon>Streptococcus mutans</taxon></cross_references></HashMap>