{"database":"GEO","file_versions":[{"headers":{"Content-Type":["application/json"]},"body":{"files":{"Other":["ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE310nnn/GSE310133/"]},"type":"primary"},"statusCode":"OK","statusCodeValue":200}],"scores":null,"additional":{"omics_type":["Transcriptomics"],"species":["Saccharomyces cerevisiae S288C"],"gds_type":["Expression profiling by high throughput sequencing"],"full_dataset_link":["https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE310133"],"repository":["GEO"],"entry_type":["GSE"],"additional_accession":[]},"is_claimable":false,"name":"The Oxidative Cost of Losing Low Temperature Viability Protein 1 [Ltv1]: Insights into Cellular Damage and Homeostasis","description":"The Ltv1 protein has been characterized with roles in ribosome biogenesis, maintenance of rRNA stability, ATP export, osmotic stress response, and signaling activation of the Target of Rapamycin pathway. We have conducted an in-depth characterization of ltv1Δ/ltv1Δ mutants for additional phenotypic manifestations due to loss of Ltv1. We observed growth differences corresponding with Ltv1’s well characterized roles but additionally discovered increased sensitivity to reactive oxygen species (ROS)-inducing conditions sodium selenite and diamide. In further characterization of cells lacking Ltv1 we documented higher levels of endogenous ROS and a greater accumulation response of ROS to exogenous stress. Utilizing RNA-sequencing we then determined the gene expression differences underlying the ltv1-deficiency induced oxidative stress sensitivity. This work elucidates a new significant role of Ltv1 in cellular homeostasis and protection against damage.","dates":{"publication":"2026/06/01"},"accession":"GSE310133","cross_references":{"GSM":["GSM9289249","GSM9289254","GSM9289252","GSM9289253","GSM9289250","GSM9289251"],"GPL":["28175"],"GSE":["310133"],"taxon":["Saccharomyces cerevisiae S288C"]}}