# Nuclear Dynamics in Quiescent Cells: Conserved Mechanisms from Yeasts to Mammals

**Authors:** Sigurd Braun, Cornelia Kilchert, Aydan Bulut-Karslioglu, Myriam Ruault, Angela Taddei, Fatemeh Rabbani, Dominika Włoch-Salamon

PMC · DOI: 10.3390/biom16020203 · Biomolecules · 2026-01-28

## TL;DR

This paper reviews how cells in a non-growing state maintain survival through nuclear changes, from yeast to mammals.

## Contribution

It highlights conserved nuclear mechanisms in quiescence, integrating metabolic state with cellular function.

## Key findings

- Quiescence involves global transcriptional repression and chromatin compaction.
- Nuclear organization changes like nucleolar condensation support long-term viability.
- TOR/mTOR signaling coordinates quiescence across species.

## Abstract

Quiescence is a reversible, non-proliferative cellular state that enables survival under nutrient limitation while preserving the capacity to resume growth. Rather than representing a passive default, quiescence is an actively regulated program conserved from unicellular eukaryotes to metazoans. This review focuses on the nuclear mechanisms underlying quiescence entry, maintenance, and exit, with primary emphasis on mechanistic insights from yeast models while highlighting conserved principles in multicellular systems. Across species, quiescence is characterized by global transcriptional repression, chromatin compaction, and the extensive reorganization of nuclear architecture, coordinated by nutrient-sensing pathways centered on TOR/mTOR signaling. We discuss how transcriptional reprogramming is achieved through redistribution of RNA polymerases, dynamic transcription factor activities, and large-scale remodeling of histone modifications, alongside repressive chromatin formation. In parallel, post-transcriptional mechanisms—including intron retention, alternative polyadenylation, and accumulation of non-coding RNAs—fine-tune gene expression while limiting biosynthetic output. We further examine how changes in nuclear organization, such as nucleolar condensation, condensin-mediated chromosome rearrangements, and telomere hyperclusters, support long-term viability and genome stability. Collectively, this review highlights nuclear dynamics as an integrative regulatory layer that links metabolic state to cellular identity, adaptability, and long-term survival, with broad implications for development, stem cell function, and disease.

## Full-text entities

- **Genes:** Crtc2 (CREB regulated transcription coactivator 2) [NCBI Gene 74343] {aka 4632407F12Rik, Torc2}, RAP1 (DNA-binding transcription factor RAP1) [NCBI Gene 855505] {aka GRC4, GRF1, TBA1, TUF1}, Crtc1 (CREB regulated transcription coactivator 1) [NCBI Gene 382056] {aka Mect1, TORC-1, TORC1, mKIAA0616}, XBP1 (Xbp1p) [NCBI Gene 854706], HHO1 (histone H1) [NCBI Gene 855976], RPS22B (40S ribosomal protein uS8 RPS22B) [NCBI Gene 851082], UBI4 (ubiquitin) [NCBI Gene 850620] {aka SCD2, UB14}, PHO85 (cyclin-dependent serine/threonine-protein kinase PHO85) [NCBI Gene 856076] {aka LDB15}, CLN3 (cyclin CLN3) [NCBI Gene 851191] {aka DAF1, FUN10, WHI1}, SET2 (histone methyltransferase SET2) [NCBI Gene 853271] {aka EZL1, KMT3}, ATF1 (alcohol O-acetyltransferase) [NCBI Gene 854559], RPS6KB1 (ribosomal protein S6 kinase B1) [NCBI Gene 6198] {aka PS6K, S6K, S6K-beta-1, S6K1, STK14A, p70 S6KA}, NAM8 (Nam8p) [NCBI Gene 856486] {aka MRE2, MUD15}, MSN2 (stress-responsive transcriptional activator MSN2) [NCBI Gene 855053], Mtor (mechanistic target of rapamycin kinase) [NCBI Gene 56717] {aka 2610315D21Rik, FRAP, FRAP2, Frap1, RAFT1, RAPT1}, DICER1 (dicer 1, ribonuclease III) [NCBI Gene 23405] {aka DCR1, Dicer, Dicer1e, GLOW, HERNA, K12H4.8-LIKE}, UME1 (Ume1p) [NCBI Gene 855964] {aka WTM3}, STB3 (Stb3p) [NCBI Gene 851747], HPA2 (histone acetyltransferase) [NCBI Gene 856323] {aka KAT10}, GID8 (glucose-induced degradation complex subunit GID8) [NCBI Gene 855166] {aka DCR1}, ESC1 (Esc1p) [NCBI Gene 855259], EHMT2 (euchromatic histone lysine methyltransferase 2) [NCBI Gene 10919] {aka BAT8, C6orf30, G9A, GAT8, KMT1C, NG36}, HHT2 (histone H3) [NCBI Gene 855700], MSN4 (stress-responsive transcriptional activator MSN4) [NCBI Gene 853803], SWI6 (transcriptional regulator SWI6) [NCBI Gene 850879] {aka PSL8, SDS11}, MUD1 (Mud1p) [NCBI Gene 852416], SIR4 (chromatin-silencing protein SIR4) [NCBI Gene 851813] {aka ASD1, STE9, UTH2}, SET1 (histone methyltransferase SET1) [NCBI Gene 856519] {aka KMT2, YTX1}, MIG2 (Mig2p) [NCBI Gene 852663] {aka MLZ1}, ATP6 (F1F0 ATP synthase subunit a) [NCBI Gene 854601] {aka OLI2, OLI4, PHO1}, FBP1 (fructose 1,6-bisphosphate 1-phosphatase) [NCBI Gene 851092] {aka ACN8}, PAF1 (Paf1p) [NCBI Gene 852582], COIL (coilin) [NCBI Gene 8161] {aka CLN80, p80-coilin}, tor (tortured) [NCBI Gene 21977], MIG3 (Mig3p) [NCBI Gene 856750], MIG1 (transcription factor MIG1) [NCBI Gene 852848] {aka CAT4, SSN1, TDS22}, SRPK2 (SRSF protein kinase 2) [NCBI Gene 6733] {aka SFRSK2}, RPD3 (histone deacetylase RPD3) [NCBI Gene 855386] {aka MOF6, REC3, SDI2, SDS6}, SIR3 (chromatin-silencing protein SIR3) [NCBI Gene 851163] {aka CMT1, MAR2, STE8}, ASP1 (asparaginase ASP1) [NCBI Gene 851920]
- **Diseases:** inflammation (MESH:D007249), injury to (MESH:D014947), cancer (MESH:D009369), DS (MESH:D020178), Fission (OMIM:614388), breast cancer (MESH:D001943), hypoxic (MESH:D002534), fungal (MESH:D009181)
- **Chemicals:** BioRender (-), GTP (MESH:D006160), phosphate (MESH:D010710), amino acids (MESH:D000596), nitrogen (MESH:D009584), carbohydrate (MESH:D002241), carbon (MESH:D002244), rapamycin (MESH:D020123), ATP (MESH:D000255), water (MESH:D014867), polyamine (MESH:D011073), acetyl-CoA (MESH:D000105), lipid (MESH:D008055), glycogen (MESH:D006003), 1,10-phenanthroline (MESH:C025205), acetate (MESH:D000085), glyoxylate (MESH:C031150), trehalose (MESH:D014199), glucose (MESH:D005947), ethanol (MESH:D000431)
- **Species:** Schizosaccharomyces pombe (fission yeast, species) [taxon 4896], Mus musculus (house mouse, species) [taxon 10090], Homo sapiens (human, species) [taxon 9606], Saccharomyces cerevisiae (baker's yeast, species) [taxon 4932], C. elegans [taxon 328850], Drosophila melanogaster (fruit fly, species) [taxon 7227]
- **Cell lines:** -MTAB-1154 — Homo sapiens (Human), Finite cell line (CVCL_4J24), NIH 3T3 — Mus musculus (Mouse), Spontaneously immortalized cell line (CVCL_0594), NQ — Homo sapiens (Human), Colon carcinoma, Cancer cell line (CVCL_H585)

## Full text

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## Figures

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## References

188 references — full list in the complete paper: https://tomesphere.com/paper/PMC12937744/full.md

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Source: https://tomesphere.com/paper/PMC12937744