Cells accumulate damaged proteins during aging and, by compromising the function of chaperones in folding newly synthesized G1 cyclins, proteostasis breakdown inhibits cell-cycle entry and drives yeast cells into senescence.
Mucins, long associated with cancer aggression, remodel the cancer glycocalyx in a way that promotes proliferation in the metastatic site by enhancing integrin-mediated adhesion and thus driving cell cycle progression.
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.
A c-Myc-transcribed long noncoding RNA namely LAST (LncRNA-assisted stabilization of transcripts) collaborates with a cellular factor CNBP to promote the stability of CCND1/cyclin D1 mRNA post-transcriptionally, ensuring the proper G1/Sphase transition of the cell cycle.
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.