<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/GSE348nnn/GSE348149/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Genomics</omics_type><species>Schizosaccharomyces pombe</species><gds_type>Genome binding/occupancy profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE348149</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>Transcription termination safeguards quiescent chromatin for faithful cell-cycle re-entry.</name><description>Quiescence is a conserved program of endurance and readiness in non-cycling cells that is fundamental to the longevity of eukaryotic lineages, from clonal microbial populations to human regenerative tissues. While this G₀ state is universally associated with a compact chromatin organization, the active safeguards that preserve this structural template—and their necessity for future division competence and fidelity—remain unknown. Here we show, using fission yeast as a model, that chromatin structural maintenance in quiescence requires the enforcement of transcription termination by the conserved factor Ppn1PNUTS/Ref2. We identify a minimal disordered region in Ppn1 that resolves a physical conflict in the quiescent genome by preventing the transcriptional “eviction” of cohesin. Loss of this safeguard drives a progressive structural erosion that deregulates cyclin dependent kinase (CDK) dynamics and causes lethal aneuploidy upon cell-cycle re-entry. Notably, this deterioration is not an inevitable terminal state; re-establishing termination via a brief Ppn1 pulse resets division fidelity by stabilizing a core de novo cohesin landscape. These findings redefine quiescent chromatin as an actively maintainable blueprint rather than a passive standby state established at G₀ entry. We propose that "quiescence exhaustion" is driven by transcriptional stress eroding genomic organization, defining a structural limit to cellular longevity.</description><dates><publication>2026/09/25</publication></dates><accession>GSE348149</accession><cross_references><GSM>GSM10067135</GSM><GSM>GSM10067136</GSM><GSM>GSM10067139</GSM><GSM>GSM10067137</GSM><GSM>GSM10067138</GSM><GSM>GSM10067142</GSM><GSM>GSM10067140</GSM><GSM>GSM10067141</GSM><GPL>28961</GPL><GSE>348149</GSE><taxon>Schizosaccharomyces pombe</taxon></cross_references></HashMap>