Mecp2 expression is cell cycle-dependent and negatively regulates quiescence exit.

In quiescent yeast, a stable bundle of parallel microtubules is assembled from the centrosome by an original multistep mechanism that follows a precise temporality and involves Aurora B and various kinesins.

Multiple mechanisms, by which a highly conserved chromatin-remodeling factor RSC facilitates initiation and maintenance of large-scale, rapid gene expression upon exit from quiescent state, have been discovered.

Application of a live-cell reporter for CDK4/6 activity reveals rapid activity changes and reversibility in the cell-cycle entry signaling program.

C. elegans germline stem cells become quiescent under starved conditions, and this quiescence maintains the stem cell state even in the absence of GLP-1/Notch signaling, which is otherwise essential for stem cell maintenance.

Lin37 is essential for cell-cycle gene repression by the DREAM complex in cellular quiescence and a combined loss of Lin37 and Rb prevents cell-cycle exit in response to growth-limiting signals.

During organismal development, CDK activity at mitotic exit is predictive of future cell behavior, indicating whether a cell will divide again or enter a quiescent state.

A new imaging approach can distinguish between cells destined to stop proliferating and those committed to re-entering the cell cycle in live animals.

The protein Tristetraprolin promotes the decay of MyoD mRNA to maintain satellite cell quiescence.

Mitochondria morphology can be use to identify quiescent and senescent yeast cells.