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Telomeres and Telomerase02:41

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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...
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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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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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An organism’s genome needs to be duplicated in an efficient and error-free manner for its growth and survival. The replication fork is a Y-shaped active region where two strands of DNA are separated and replicated continuously. The coupling of DNA unzipping and complementary strand synthesis is a characteristic feature of a replication fork.   Organisms with small circular DNA, such as E. coli, often have a single origin of replication; therefore, they have only two replication...
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DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart,...
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Before a cell can divide, it must accurately replicate all of its chromosomes, including the DNA and its associated histone and non-histone proteins.  This process begins at numerous origins of replication during the S phase of the cell cycle in each of a cell’s chromosomes simultaneously. Certain nucleotides can act as origins of replication, but these sequences are not well defined - especially in complex, multi-cellular, eukaryotic species. The length of DNA that spans an origin...
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Utilizing Murine Inducible Telomerase Alleles in the Studies of Tissue Degeneration/Regeneration and Cancer
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Consequences of telomere replication failure: the other end-replication problem.

Kirsten A Brenner1, Jayakrishnan Nandakumar1

  • 1Department of Molecular, Cellular, and Developmental Biology, University of Michigan, Ann Arbor, MI 48109, USA.

Trends in Biochemical Sciences
|April 20, 2022
PubMed
Summary
This summary is machine-generated.

Replication stress at telomeres (chromosome ends) can lead to genomic instability. While repair mechanisms exist, they are error-prone and may promote cancer, suggesting unrepaired telomeres could be tumor-suppressive.

Keywords:
alternative lengthening of telomeresbreak-induced replicationmitotic DNA synthesisreplication stresstelomeres

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Area of Science:

  • Genetics
  • Molecular Biology
  • Cell Biology

Background:

  • Telomeres cap chromosome ends, protecting the genome but posing replication challenges.
  • Incomplete replication shortens telomeres, limiting cell lifespan and requiring repair pathways.
  • Replication stress at telomeres can trigger error-prone break-induced replication (BIR) and mitotic DNA synthesis (MiDAS).

Purpose of the Study:

  • To review the consequences of replication stress at mammalian telomeres.
  • To discuss how DNA repair pathways at telomeres contribute to genomic instability.
  • To explore the implications of telomere fragility in cancer development.

Main Methods:

  • Literature review of recent findings on telomere replication and repair.
  • Analysis of mechanisms like BIR and MiDAS in response to replication stress.
  • Discussion of the link between telomere instability and tumorigenesis.

Main Results:

  • Replication stress at telomeres activates error-prone repair pathways (BIR, MiDAS).
  • These pathways, while attempting repair, contribute to genomic instability.
  • Fragile telomeres are primarily observed in cancer cells.

Conclusions:

  • Telomere repair mechanisms under replication stress are often mutagenic.
  • Telomere fragility may act as a tumor-suppressive mechanism.
  • Leaving telomeres unrepaired might be a strategy to prevent cancer progression.