Translational Control during Cellular Senescence

Mol Cell Biol. 2021 Jan 25;41(2):e00512-20. doi: 10.1128/MCB.00512-20. Print 2021 Jan 25.


Senescence is a state of long-term cell cycle arrest that arises in cells that have incurred sublethal damage. While senescent cells no longer replicate, they remain metabolically active and further develop unique and stable phenotypes that are not present in proliferating cells. On one hand, senescent cells increase in size, maintain an active mTORC1 complex, and produce and secrete a substantial amount of inflammatory proteins as part of the senescence-associated secretory phenotype (SASP). On the other hand, these progrowth phenotypes contrast with the p53-mediated growth arrest typical of senescent cells that is associated with nucleolar stress and an inhibition of rRNA processing and ribosome biogenesis. In sum, translation in senescent cells paradoxically comprises both a global repression of translation triggered by DNA damage and a select increase in the translation of specific proteins, including SASP factors.

Keywords: aging; cellular senescence; stress response; translation elongation; translation initiation; translational control.

Publication types

  • Research Support, N.I.H., Intramural
  • Review

MeSH terms

  • Biomarkers / metabolism
  • Cell Size
  • Cells, Cultured
  • Cellular Senescence / genetics*
  • Chemokines / genetics*
  • Chemokines / metabolism
  • Cyclin-Dependent Kinase Inhibitor p21 / genetics
  • Cyclin-Dependent Kinase Inhibitor p21 / metabolism
  • DNA Damage
  • Humans
  • Mechanistic Target of Rapamycin Complex 1 / genetics*
  • Mechanistic Target of Rapamycin Complex 1 / metabolism
  • Phenotype
  • Protein Biosynthesis*
  • RNA, Ribosomal / genetics
  • RNA, Ribosomal / metabolism
  • Tumor Suppressor Protein p53 / genetics*
  • Tumor Suppressor Protein p53 / metabolism
  • beta-Galactosidase / genetics
  • beta-Galactosidase / metabolism


  • Biomarkers
  • Chemokines
  • Cyclin-Dependent Kinase Inhibitor p21
  • RNA, Ribosomal
  • Tumor Suppressor Protein p53
  • Mechanistic Target of Rapamycin Complex 1
  • beta-Galactosidase