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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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Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence
12:08

Telomere Length and Telomerase Activity; A Yin and Yang of Cell Senescence

Published on: May 22, 2013

A computational model for telomere-dependent cell-replicative aging.

R D Portugal1, M G P Land, B F Svaiter

  • 1Hematology Service, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil.

Bio Systems
|December 8, 2007
PubMed
Summary

Telomere shortening, the progressive shortening of chromosome ends, influences cell division rates. A new stochastic model accurately simulates how this process affects human stem cell growth.

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Area of Science:

  • Cell Biology
  • Biophysics
  • Computational Biology

Background:

  • Telomere shortening is linked to cellular aging and the Hayflick limit.
  • Emerging evidence suggests telomere length impacts cell division rates.
  • Understanding this relationship is crucial for regenerative medicine and aging research.

Purpose of the Study:

  • To propose and validate a stochastic growth model for cell division regulated by telomere shortening.
  • To investigate the quantitative relationship between telomere length and mitotic probability.
  • To simulate the growth dynamics of human mesenchymal stem cells under telomere-dependent regulation.

Main Methods:

  • Developed a stochastic growth model where cell division probability decreases linearly with telomere shortening.
  • Employed computer simulations to analyze the model's predictions.
  • Compared simulation results with qualitative growth patterns of cultured human mesenchymal stem cells.

Main Results:

  • The proposed stochastic model effectively captures the qualitative growth dynamics of human mesenchymal stem cells.
  • Simulation results show good approximation of cell proliferation influenced by telomere shortening.
  • The model provides a framework for understanding telomere-regulated mitotic rates.

Conclusions:

  • Telomere shortening is a significant factor influencing cellular mitotic rates.
  • The developed stochastic model offers a valuable tool for studying cell proliferation and aging.
  • This research contributes to a deeper understanding of the molecular mechanisms underlying cellular senescence and stem cell behavior.