Cell-cycle exit articles from across Nature Portfolio

Unveiling the regulation of mitotic protein degradation is crucial for cancer therapy. Here, the authors reveal that a reciprocal inhibition of PIN1-APC/C^CDH1 controls the cell cycle and mitotic protein degradation, offering a synergistic anti-tumor strategy.

Metastasis arises from disseminated tumour cells (DTCs) while the underlying mechanism of DTCs plasticity remains underexplored. Here, the authors show that spatially organized oncogenic enhancers on chromatin sustain the establishment of retinoic acid (RA)-stimulated transcriptional memory through activation of SOX9, supporting the escape of quiescent DTCs from NK-mediated immune surveillance.

Plasma membrane damage (PMD) can induce cell death or be repaired, whereas other cell fates are not well explored. In this study, the authors found that PMD induces senescence in yeast and human fibroblasts in a manner that is distinct from DNA damage-dependent senescence. They present transcriptomic data suggesting that this PMD response may explain the origins of senescent cells near cutaneous wounds.

Cyclin-dependent kinases (CDK4/6) play a crucial role in initiating cell growth. Here, Zhang et al. unveil a mechanism that bypasses CDK4/6, shedding light on an alternative pathway of cell-cycle initiation and quiescence maintenance.

Systematic examination of H2b-GFP label retaining cells in mouse digestive organ uncovered a slow-cycling subpopulation of gastric chief cells that uniquely express markers of paligenosis and are ready to undergo proliferation after external damage.

The onset of differentiation has been assumed to follow withdrawal from the cell cycle. A new study shows that keratinocytes initiate differentiation before exiting the cell cycle, allowing the skin to respond rapidly to damage.

Mitotic exit follows shortly after microtubule attachment of the last unattached kinetochore. Two new studies illustrate the molecular basis of this dependency.

Repo-Man has a role in both chromatin remodelling and nuclear envelope reformation.