<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/GSE336nnn/GSE336602/</Other></files><type>primary</type></body><statusCodeValue>200</statusCodeValue><statusCode>OK</statusCode></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Clostridioides difficile</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=GSE336602</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Effect of curing the phi027 prophage for gene expresson in Clostridioides difficile clinical isolate 500/12</name><description>Clostridioides difficile is a clinically important nosocomial pathogen whose virulence is primarily associated with toxin production and can be influenced by prophage carriage. In this study, we investigated the molecular basis of phi027-dependent phenotypic differences previously observed between the clinical RT176 strain 500/12 and its prophage-free derivative CKH08. Comparative transcriptomic analysis revealed that loss of phi027 was associated with reduced expression of the sinR/R' operon, downregulation of multiple flagellar biosynthesis genes.</description><dates><publication>2026/07/01</publication></dates><accession>GSE336602</accession><cross_references><GSM>GSM9838636</GSM><GSM>GSM9838637</GSM><GSM>GSM9838638</GSM><GSM>GSM9838639</GSM><GSM>GSM9838643</GSM><GSM>GSM9838640</GSM><GSM>GSM9838641</GSM><GSM>GSM9838642</GSM><GPL>30071</GPL><GSE>336602</GSE><taxon>Clostridioides difficile</taxon></cross_references></HashMap>