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

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.

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

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.

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.

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.

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

A molecular duel between germline and somatic determinants ensures proper establishment of transcriptional quiescence in the primordial germ cells of early Drosophila embryos.

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

The stem cells of the postnatal muscle allow postnatal muscle growth and repair and withdraw from the cell cycle when the tyrosine phosphatase Ptpn11 (Shp2) is inhibited or mutated in mice.