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Replicative Cell Senescence

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 Eukaryotes

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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.
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Replication in Eukaryotes

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Telomeres and Telomerase

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 Telomerase

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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.

DNA Damage can Stall the Cell Cycle

DNA Damage can Stall the Cell Cycle

In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...

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Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer

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Published on: April 13, 2015

Defective Artemis causes mild telomere dysfunction.

Hemad Yasaei¹, Predrag Slijepcevic

¹Brunel Institute of Cancer Genetics and Pharmacogenomics, Division of Biosciences, School of Health Sciences and Social Care, Brunel University, Uxbridge, Middlesex, UB8 3PH, UK. predrag.slijepcevic@brunel.ac.uk.

Genome Integrity

|August 4, 2010

Summary

This summary is machine-generated.

Defective Artemis impairs telomere maintenance, leading to increased telomeric fusions and DNA damage in human cells. This suggests Artemis plays a role in preventing telomere dysfunction.

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

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

Published on: May 22, 2013

Area of Science:

Molecular Biology
Genetics
Cell Biology

Background:

Non-homologous end joining (NHEJ) repairs DNA double-strand breaks using proteins like Ku, DNA-PKcs, Artemis, XRCC4, Ligase IV, and XLF.
Ku and DNA-PKcs are implicated in telomere maintenance, while XRCC4 and Ligase IV are not.
Previous studies suggested Artemis deficiency might lead to telomere dysfunction.

Purpose of the Study:

To investigate the impact of Artemis deficiency on telomere maintenance in human cells.

Main Methods:

Analysis of telomeric fusions in primary fibroblast cell lines from Artemis-deficient patients.
Assessment of telomere dysfunction using the TIF (Telomere dysfunction Induced Foci) assay.
Inhibition of DNA-PKcs expression in Artemis-deficient cells using a synthetic inhibitor (IC86621) and RNA interference (RNAi).

Main Results:

Artemis-deficient cells exhibited significantly higher frequencies of telomeric fusions compared to control cells.
Telomeric fusion frequencies increased in Artemis-deficient cells upon exposure to ionizing radiation.
Elevated DNA damage at telomeres was observed in late-passage Artemis-deficient cells.
Artemis-deficient cells showed increased sensitivity to telomere dysfunction when DNA-PKcs was inhibited.

Conclusions:

Defective Artemis leads to a mild telomere dysfunction phenotype in human cell lines.
These findings highlight a role for Artemis in maintaining telomere stability.