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Related Concept Videos

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.
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...
Fixing Double-strand Breaks02:04

Fixing Double-strand Breaks

The double-stranded structure of DNA has two major advantages. First, it serves as a safe repository of genetic information where one strand serves as the back-up in case the other strand is damaged. Second, the double-helical structure can be wrapped around proteins called histones to form nucleosomes, which can then be tightly wound to form chromosomes. This way, DNA chains up to 2 inches long can be contained within microscopic structures in a cell. A double-stranded break not only damages...

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Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
08:34

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Published on: April 13, 2015

Telomere maintenance and human bone marrow failure.

Rodrigo T Calado1, Neal S Young

  • 1Hematology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA. calador@nhlbi.nih.gov

Blood
|February 2, 2008
PubMed
Summary
This summary is machine-generated.

Abnormal telomere maintenance links aplastic anemias. Short telomeres, caused by telomerase gene mutations or other factors, impair hematopoietic stem cell function and may lead to marrow failure syndromes.

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Published on: January 26, 2024

Area of Science:

  • Genetics
  • Hematology
  • Molecular Biology

Background:

  • Telomeres protect chromosome ends but shorten with cell division.
  • Hematopoietic stem cell telomere length is maintained by telomerase.
  • Dyskeratosis congenita and aplastic anemia share links to abnormal telomere maintenance.

Purpose of the Study:

  • To explore the molecular and pathophysiological links between aplastic anemias and telomere maintenance.
  • To investigate the role of telomere shortening in hematopoietic stem cell dysfunction.
  • To identify the clinical implications of short telomeres in marrow failure syndromes.

Main Methods:

  • Analysis of telomere length in patients with aplastic anemias.
  • Genetic analysis of genes involved in telomere maintenance (TERT, TERC, DKC1, NOP10, TINF2).
  • Assessment of telomerase activity and hematopoietic progenitor proliferation.

Main Results:

  • Accelerated telomere shortening is common in dyskeratosis congenita due to telomerase gene mutations.
  • Approximately one-third of aplastic anemia patients have short telomeres, sometimes linked to TERT/TERC mutations.
  • Short telomeres lead to reduced telomerase activity, accelerated shortening, and impaired hematopoietic progenitor proliferation.

Conclusions:

  • Abnormal telomere maintenance is a unifying factor in acquired and congenital aplastic anemias.
  • Short telomeres can cause genomic instability and malignant progression.
  • Identifying short telomeres aids in diagnosing dyskeratosis congenita, suggesting mutations in aplastic anemia, and selecting stem cell donors.