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.
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 LIN37-DREAM complex has a critical role in regulating DNA double-strand break end processing and suppressing aberrant homology-directed repair in quiescent cells.
A molecular duel between germline and somatic determinants ensures proper establishment of transcriptional quiescence in the primordial germ cells of early Drosophila embryos.
