MicroRNAs tightly control the cellular level of homologous recombination (HR) factors in the G1 phase, and failure of this control system results in an ectopic increase in HR proteins in G1 cells leading to impaired DNA repair.

The retinoblastoma tumor suppressor regulates cell cycle progression when it's in 14 mono-phosphorylated isoforms.

The regulation of the core transcription factor Oct4 by the Aurkb-PP1 axis links the cell cycle to pluripotency programs in embryonic stem cells.

mRNA decay contributes to reshape the transcriptome as a parent cell divides into daughter cells.

The RIF1-long and short splice variants show distinct ability to protect cells from replication stress by promoting 53BP1 nuclear bodies, representing the first described functional difference between the two variants.

The unique cell cycle variations of pluripotent stem cells ensures that the first step in DNA replication is particularly fast and this rapid rate, in turn, restrains early differentiation.

During tumorigenesis loss of p53 not only abrogates cell cycle arrest and apoptosis, but also suppresses the induction of replication-stress-induced DNA double-stranded breaks.

In G1 cells, Scc2 loads and maintains cohesin on chromosomes by counteracting a Wapl-independent releasing activity, which is neutralized in S phase by CDK1.

Cell imaging and mathematical modelling show reciprocal cross-regulation between inflammatory signalling and cell cycle timing, which is mediated through functional interactions between NF-B and E2F proteins.

A multi-layered and conserved cell cycle mechanism prevents capsulation, long known as a bacterial virulence determinant, in G1-phase and concurrently licenses bacteriophage-mediated genetic exchange prior to entry into S-phase.