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Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

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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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Replication in Eukaryotes01:29

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In eukaryotic cells, DNA replication is highly conserved and tightly regulated. Multiple linear chromosomes must be duplicated with high fidelity before cell division, so there are many proteins that fulfill specialized roles in the replication process. Replication occurs in three phases: initiation, elongation, and termination, and ends with two complete sets of chromosomes in the nucleus.
Many Proteins Orchestrate Replication at the Origin
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Improving Translational Accuracy02:07

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Base complementarity between the three base pairs of mRNA codon and the tRNA anticodon is not a failsafe mechanism. Inaccuracies can range from a single mismatch to no correct base pairing at all. The free energy difference between the correct and nearly correct base pairs can be as small as 3 kcal/ mol. With complementarity being the only proofreading step, the estimated error frequency would be one wrong amino acid in every 100 amino acids incorporated. However, error frequencies observed in...
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Regulation of Expression Occurs at Multiple Steps02:24

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Gene expression can be regulated at almost every step from gene to protein. Transcription is the step that is most commonly regulated. This involves the binding of proteins to short regulatory sequences on the DNA. This association can either promote or inhibit the transcription of a gene associated with the respective sequence.
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Nonsense-mediated mRNA Decay02:27

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The Upf proteins that carry out nonsense-mediated decay (NMD) are found in all eukaryotic organisms, including humans. Each protein has an individual role, but they need to work in collaboration. Upf1 is an ATP-dependent RNA helicase that unwinds the RNA helix. Because Upf1 can unwind any RNA, Upf2 and Upf3 are required to help Upf1 discriminate between nonsense and normal mRNAs.
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Before mRNAs are exported to the cytoplasm, it is crucial to check each mRNA for structural and functional integrity. Eukaryotic cells use several different mechanisms, collectively known as mRNA surveillance, to look for irregularities in mRNAs. Irregular or aberrant mRNA are rapidly degraded by various enzymes. If a defective mRNA escapes the surveillance, it would be translated into a protein which would either be non-functional or not function properly. One of the primary irregularities in...
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Updated: Oct 16, 2025

Techniques to Induce and Quantify Cellular Senescence
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Techniques to Induce and Quantify Cellular Senescence

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Cellular senescence limits translational readthrough.

Neylen Del Toro1, Frédéric Lessard1, Jacob Bouchard1

  • 1Département de Biochimie et Médecine Moléculaire, Université de Montréal C.P. 6128, Succ. Centre-Ville, Montréal, Québec, H3C 3J7, Canada.

Biology Open
|October 22, 2021
PubMed
Summary
This summary is machine-generated.

Cellular senescence, a cancer-preventing process, reduces translational readthrough (TR) errors. Escaping senescence increases TR, potentially driving cancer progression by enhancing proteome diversity and proliferation.

Keywords:
Retinoblastoma (RB) tumor suppressorSenescenceTranslation terminationTranslational readthrough

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Area of Science:

  • Molecular Biology
  • Cancer Biology
  • Genetics

Background:

  • Cancer development is primarily linked to DNA mutations.
  • The role of translation errors in cancer remains unclear.
  • Caretaker tumor suppressors prevent DNA mutations and promote repair.

Purpose of the Study:

  • Investigate if caretaker genes prevent translation errors during oncogenic stress.
  • Determine the effect of cellular senescence on translational readthrough (TR).
  • Elucidate the role of TR in cancer cell proliferation and escape from senescence.

Main Methods:

  • Utilized reporter assays to measure translational readthrough (TR).
  • Induced cellular senescence using oncogenes, tumor suppressors, and chemotherapy.
  • Analyzed the RB tumor suppressor pathway's role in regulating TR during senescence.
  • Assessed TR levels in cells escaping senescence and in breast cancer cells.

Main Results:

  • Cellular senescence significantly reduces both basal and aminoglycoside-stimulated TR.
  • The RB tumor suppressor pathway mechanistically controls TR reduction during senescence.
  • Cells evading oncogene- or chemotherapy-induced senescence exhibit increased TR.
  • Breast cancer cells that escape therapy-induced senescence overexpress AGO1x, a TR isoform linked to progression.

Conclusions:

  • Senescence and the RB pathway suppress TR, limiting proteome diversity.
  • Reduced TR may prevent the expression of TR proteins essential for cancer cell proliferation.
  • Increased TR in senescence-escaped cells could contribute to cancer progression.