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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.
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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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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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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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ATR blocks telomerase from converting DNA breaks into telomeres.

Charles G Kinzig1,2, George Zakusilo1,2, Kaori K Takai1

  • 1Laboratory for Cell Biology and Genetics, The Rockefeller University, New York, NY 10065, USA.

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Telomerase can add telomeric repeats to DNA double-strand breaks (DSBs), potentially harming genome integrity. However, ATR kinase signaling inhibits telomerase at resected DSBs, protecting cells.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Telomeres protect chromosome ends, and telomerase maintains their length.
  • Telomerase activity at DNA double-strand breaks (DSBs) can lead to genome instability.
  • Neotelomere formation at DSBs can result in terminal truncations.

Purpose of the Study:

  • To investigate the role of telomerase at induced DSBs in human cells.
  • To identify mechanisms that regulate telomerase activity at DSBs.
  • To understand the implications of neotelomere formation for genome integrity.

Main Methods:

  • Developed a novel assay to detect neotelomere formation at Cas9- or I-SceI-induced DSBs.
  • Utilized human cell lines for experimental analysis.
  • Investigated the role of ataxia telangiectasia and Rad3-related (ATR) kinase signaling.

Main Results:

  • Telomerase was found to add telomeric repeats to DSBs, causing interstitial telomeric repeat insertions or functional neotelomeres with terminal deletions.
  • ATR kinase signaling inhibited telomerase activity at resected DSBs, mitigating the threat to genome integrity.
  • Telomerase utilized extruded strands in Cas9 enzyme-product complexes as primers for neotelomere formation.

Conclusions:

  • Neotelomere formation by telomerase poses a threat to genome integrity in normal human cells.
  • ATR-mediated inhibition of telomerase at DSBs is a crucial protective mechanism.
  • Neotelomere formation may provide a survival advantage for cancer cells by preventing breakage-fusion-bridge cycles.