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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

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.

Replication in Eukaryotes

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 Eukaryotes

Replication in Eukaryotes

Mismatch Repair

Mismatch Repair

Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...

Mismatch Repair

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Related Experiment Video

Updated: Jun 21, 2026

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

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Published on: June 26, 2020

Multiple roles for MRE11 at uncapped telomeres.

Yibin Deng¹, Xiaolan Guo, David O Ferguson

¹Department of Genetics, Box 1010, The M.D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, Texas 77030, USA.

|July 28, 2009

Summary

The MRN complex is crucial for sensing dysfunctional telomeres and promoting DNA repair. MRE11 nuclease activity prevents harmful chromosome fusions by processing telomeric overhangs.

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Area of Science:

Genetics
Molecular Biology
Cell Biology

Background:

Telomere dysfunction triggers DNA damage responses, mimicking double-strand breaks.
The MRN complex (MRE11-RAD50-NBS1) is known to sense DNA breaks but its role at telomeres is unclear.

Purpose of the Study:

To investigate the role of the MRN complex in sensing dysfunctional telomeres and promoting repair.
To determine if MRE11 nuclease activity is required for telomere maintenance and preventing chromosome fusions.

Main Methods:

Utilized mouse models with inactivated MRN complex or MRE11 nuclease activity.
Assessed ATM activation, 53BP1 recruitment, and chromosome end-to-end fusions upon telomere deprotection (TRF2 removal).
Examined the impact of MRE11 nuclease deficiency on 3' telomeric overhangs and NHEJ.

Main Results:

MRN-deficient cells failed to activate ATM and showed reduced chromosome fusions after TRF2 removal.
MRE11 nuclease-deficient cells activated ATM and recruited 53BP1 but maintained 3' overhangs, inhibiting NHEJ.
Loss of shelterin proteins in MRE11-deficient cells restored fusions, indicating MRE11's role in overhang processing.

Conclusions:

The MRN complex is essential for sensing telomere dysfunction and initiating DNA damage responses.
MRE11 nuclease activity processes 3' telomeric overhangs, preventing NHEJ-mediated chromosome fusions, and protects newly replicated telomeres.