<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/GSE294nnn/GSE294295/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Candida albicans</species><gds_type> Other</gds_type><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE294295</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Met32 governs transcriptional control of sulfur metabolic flexibility and resistance to reactive sulfur species in the human fungal pathogen Candida albicans</name><description>Although considerable advances were made in understanding the metabolic machinery that enable bacteria to utilize alternative sulfur sources, many aspects of this process remain understudied in fungi. To explore the genetic circuit by which the highly prevalent opportunistic yeast Candida albicans control sulfur utilization, we characterized the transcriptional atlas associated with sulfur starvation in this yeast. We identified many putative desulfonation enzymes that were differentially transcribed and showed that Jlp12, an α-ketoglutarate dioxygenase, was critical for the utilization of different sulfur sources found in many niches of the human host. We also uncovered that the Zinc-finger transcription factor Met32 acts as a master transcriptional regulator, that modulates genes of sulfur utilization including Jpl12. Importantly, we found that the C. albicans Met32 functions exclusively in the control of sulfur utilization genes, while it governs methionine biosynthesis in the S. cerevisiae lineage. This work also identified Seo13 as the first major facilitator superfamily transporter in fungi that transports the alternative sulfur source glutathione, under the direct control of Met32. Furthermore, we showed that Met32 modulates C. albicans tolerance sulfite excess by tuning the basal transcriptional level of the superoxide dismutase Sod1. This underscores the dual role of Met32 in the breakdown of sulfur-containing metabolites and the neutralization of the resulting reactive sulfur species (RSS). Our study delineates a new mechanism by which fungal pathogens utilize sulfur sources and neutralize RSS, and underscores its importance for fungal fitness in vivo.</description><dates><publication>2026/04/02</publication></dates><accession>GSE294295</accession><cross_references><GSM>GSM8901880</GSM><GSM>GSM8901871</GSM><GSM>GSM8901882</GSM><GSM>GSM8901860</GSM><GSM>GSM8901881</GSM><GSM>GSM8901870</GSM><GSM>GSM8901877</GSM><GSM>GSM8901865</GSM><GSM>GSM8901876</GSM><GSM>GSM8901868</GSM><GSM>GSM8901879</GSM><GSM>GSM8901867</GSM><GSM>GSM8901862</GSM><GSM>GSM8901873</GSM><GSM>GSM8901872</GSM><GSM>GSM8901861</GSM><GSM>GSM8901883</GSM><GSM>GSM8901875</GSM><GSM>GSM8901864</GSM><GSM>GSM8901863</GSM><GSM>GSM8901874</GSM><GSM>GSM8901859</GSM><GSM>GSM8901869</GSM><GSM>GSM8901858</GSM><GPL>28323</GPL><GSE>294295</GSE><taxon>Candida albicans</taxon></cross_references></HashMap>