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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
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The caspase-activated DNase promotes cellular senescence.

Aladin Haimovici1, Valentin Rupp2, Tarek Amer2

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The caspase-activated DNase (CAD) enzyme initiates cellular senescence by causing DNA damage, even without cell death. This discovery reveals CAD as a key factor in senescence across various stress responses.

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Area of Science:

  • Molecular Biology
  • Cell Biology
  • Genetics

Background:

  • Cellular senescence is a stress response characterized by DNA damage, but its origins are often unclear.
  • The enzyme caspase-activated DNase (CAD) is known to degrade DNA during apoptosis.

Purpose of the Study:

  • To identify the source of DNA damage in cellular senescence.
  • To investigate the role of CAD in initiating senescence.

Main Methods:

  • Investigated CAD activation by sub-lethal apoptotic signals.
  • Assessed senescence induction by oncogenic RAS, type-I interferon, and doxorubicin.
  • Experimentally activated CAD in human cells.
  • Studied senescence in CAD-deficient mice.

Main Results:

  • Sub-lethal apoptotic signals activate CAD, causing DNA damage and senescence without cell death.
  • CAD is essential for senescence induced by oncogenic RAS, type-I interferon, and doxorubicin.
  • Direct CAD activation is sufficient to induce senescence in human cells.
  • CAD-deficient mice show reduced senescence in aging organs.

Conclusions:

  • CAD-induced DNA damage is a critical mechanism for initiating cellular senescence.
  • CAD acts as a central mediator of senescence in response to diverse cellular insults.