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Related Concept Videos

Replicative Cell Senescence02:15

Replicative Cell Senescence

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 the telomeric...
Replicative Cell Senescence02:15

Replicative Cell Senescence

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 the telomeric...
Replication in Eukaryotes01:29

Replication in Eukaryotes

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
Eukaryotic replication follows many of the same...
Replication in Eukaryotes02:31

Replication in Eukaryotes

Overview
Telomeres and Telomerase02:41

Telomeres and Telomerase

In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded DNA.
Telomeres and Telomerase02:41

Telomeres and Telomerase

In eukaryotic DNA replication, a single-stranded DNA fragment remains at the end of a chromosome after the removal of the final primer. This section of DNA cannot be replicated in the same manner as the rest of the strand because there is no 3’ end to which the newly synthesized DNA can attach. This non-replicated fragment results in gradual loss of the chromosomal DNA during each cell duplication. Additionally, it can induce a DNA damage response by enzymes that recognize single-stranded DNA.

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Measuring Replicative Life Span in the Budding Yeast
12:41

Measuring Replicative Life Span in the Budding Yeast

Published on: June 25, 2009

Multiple genetic pathways regulate replicative senescence in telomerase-deficient yeast.

Bari J Ballew1, Victoria Lundblad

  • 1Salk Institute for Biological Studies, La Jolla, CA 92037-1099, USA.

Aging Cell
|May 16, 2013
PubMed
Summary

Telomere shortening limits tissue renewal and aging. This study reveals that DNA repair pathways, particularly the MRX complex and Rad51 recombinase, significantly influence yeast replicative senescence, offering insights into human aging.

Keywords:
MRXRad51Rif2replicative senescencetelomerasetelomeresyeast

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Area of Science:

  • Cellular Biology
  • Genetics
  • Molecular Biology

Background:

  • Telomere shortening limits cell division and contributes to age-related diseases.
  • Genetic factors influence the rate of cellular senescence in telomerase-deficient cells.

Purpose of the Study:

  • To investigate how DNA end-handling factors affect replicative senescence in telomerase-defective yeast.
  • To elucidate the genetic pathways controlling cellular aging due to telomere erosion.

Main Methods:

  • Utilized telomerase-defective budding yeast strains.
  • Examined the impact of mutations in DNA repair genes (MRX complex, Rif2, Tel1, Rad51, Rif1, Sae2) on replicative senescence.
  • Analyzed the role of these factors in DNA end resection and double-strand break (DSB) repair pathways.

Main Results:

  • The MRX complex, Tel1, and Rif2 form a pathway that promotes replicative senescence.
  • Rad51 acts in an opposing pathway to regulate senescence.
  • Rif1 and Sae2 have transient effects, indicating a complex genetic control network rather than a simple analogy between DSBs and telomere erosion.

Conclusions:

  • Cellular replicative capacity in yeast is controlled by a complex network of interacting genetic pathways.
  • Understanding these pathways provides crucial insights into how telomere shortening drives tissue aging in humans.