Genetic and protein analyses in vitro and in vivo identifies Id4 as a novel regulator of stem cell quiescence in the adult hippocampus.

Using a yeast model of quiescence, it was demonstrated that dramatic changes in local chromatin fiber folding can occur under physiological conditions to regulate cellular processes.

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.

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.

The quiescence-driven mutational landscape reveals replication-independent mutagenesis as a novel evolutionary force.

A switch-like cell fate divergence revealed by continuous single-cell tracking during entry into quiescence.

The acquisition of vascular quiescence during transition to adulthood is driven by distinct transcriptional and epigenetic programs of pro- and anti-angiogenic genes, with the most prominent effect on the suppression of TGFß family signaling.

A user-friendly, and modular, 3D skeletal muscle culture assay enables iterative studies of murine muscle stem cell pool size regulation, functional heterogeneity, return to quiescence, and age-associated functional defects within a 96-well footprint.

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 low-level pulse of the nuclear Prospero protein is necessary and sufficient to cause neural progenitor cells to enter a quiescent state.