Biology · MU Sofia

29. Cell senescence. Cell death: apoptosis, necrosis.

Covers cell senescence, from replicative ageing after roughly 50 divisions and stress-induced triggers through to the senescence-associated secretory phenotype, with ageing in budding yeast and the role of telomeres and telomerase. Moves on to programmed cell death, autophagy, and necrosis versus apoptosis, then the caspase cascade, its two activation pathways, and Bcl-2 and IAP regulation. Three mnemonics (SAGE, NAA and FICA) are included to help with comparisons.

Inside: 14 sections · 3 labelled pictures · 10 flashcards · 8 min

Topic 30 of 105 in the MU Sofia syllabus for Biology (Medicine, Year 1). The free AceMed note covers it in 14 sections, about 1,112 words (8 min of reading), with 10 flashcards.

In this note

  1. Cell senescence. Cell death: apoptosis, necrosis
  2. Cell Senescence
  3. Senescence in Budding Yeast
  4. Telomeres and Their Role in Senescence
  5. Forms of Cell Death
  6. Autophagy
  7. Necrosis versus Apoptosis
  8. Functions of Programmed Cell Death
  9. Mechanism of Apoptosis
  10. Activation of Apoptosis
  11. Regulation of Apoptosis
  12. Bcl-2 Family
  13. IAP Family
  14. MNEMONICS

Cell Senescence

  • Cell senescence is a state where normal cells permanently stop dividing, typically after around 50 divisions in laboratory conditions. This is known as replicative senescence.
  • Cells may also enter senescence due to stress factors like toxins, radiation, or activation of certain cancer-related genes.
  • When cells experience DNA damage, such as telomere shortening, they either repair the damage, self-destruct through apoptosis, or become senescent if the damage is irreparable.
  • Senescent cells are still alive and metabolically active, but they no longer divide.
  • These cells develop a distinctive pattern of gene expression and start secreting various molecules, a phenomenon known as the senescence-associated secretory phenotype.
  • They also undergo changes in shape and structure.
  • It was once believed that single-celled organisms did not experience senescence. However, it is now understood that even single cells can accumulate damage over time.
  • In some bacteria and yeast, cell division is asymmetrical. One daughter cell inherits most of the damaged components, while the other remains "young." Over time, this leads to some cells aging and others staying rejuvenated.
  • This suggests senescence may be a universal biological strategy to deal with accumulated cellular damage.

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