![]() ![]() Indeed, the majority of ‘healthy’ cells on earth are not sustained in a persistently dividing state ( Rittershaus et al., 2013). Furthermore, many cell populations in multicellular organisms, such as in humans, are not actively dividing ( Sagot and Laporte, 2019 Rittershaus et al., 2013 Cheung and Rando, 2013). Log phase, however, is not a common growth stage in unicellular organism lifecycles. Introductionįor decades, scientists have used budding yeast to uncover mechanisms of chromatin regulation of gene expression, and the vast majority of these studies were performed in exponentially growing (hereafter log) cultures ( Rando and Winston, 2012). Together, these results uncovered multiple mechanisms by which RSC facilitates initiation and maintenance of large-scale, rapid gene expression despite a globally repressive chromatin state. These phenomena were due to a combination of highly robust Pol II transcription and severe chromatin defects in the promoter regions and gene bodies. RSC depletion caused severe quiescence exit defects: a global decrease in RNA polymerase II (Pol II) loading, Pol II accumulation at transcription start sites, initiation from ectopic upstream loci, and aberrant antisense transcription. During quiescence, the chromatin-remodeling enzyme RSC was already bound to the genes induced upon quiescence exit. ![]() Here we report robust, widespread transcription within the first minutes of quiescence exit. How transcription activates upon cell-cycle re-entry is undefined. Necessary for long-term survival, quiescent chromatin is compact, hypoacetylated, and transcriptionally inactive. Quiescence is a reversible G 0 state essential for differentiation, regeneration, stem-cell renewal, and immune cell activation. ![]()
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