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Related Concept Videos

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.
DNA Damage can Stall the Cell Cycle02:36

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...
DNA Damage Can Stall the Cell Cycle02:36

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...
Mismatch Repair01:20

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 Repair01:36

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Overview
Master Transcription Regulators02:23

Master Transcription Regulators

Master transcription regulators are regulatory proteins that are predominantly responsible for regulating the expression of multiple genes. Often these genes work in concert to drive a  complex process. Activation of a master transcription regulator can lead to a cascade of transcriptional activation necessary for that outcome. These regulators can directly bind to the regulatory sequences of the various genes involved, or they can indirectly regulate transcription by binding to regulatory...

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Related Experiment Video

Updated: Jun 27, 2026

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
07:55

Visualization of DNA Repair Proteins Interaction by Immunofluorescence

Published on: June 26, 2020

Mec1 function in the DNA damage response does not require its interaction with Tel2.

Carol M Anderson1, Elizabeth H Blackburn

  • 1Department of Biochemistry and Biophysics, University of California, San Francisco, California 94158, USA.

Cell Cycle (Georgetown, Tex.)
|November 26, 2008
PubMed
Summary
This summary is machine-generated.

The Tel2 protein interacts with PIKKs, crucial for DNA damage response. Surprisingly, a tel2-1 mutation disrupts Tel2

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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
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Visualization of DNA Repair Proteins Interaction by Immunofluorescence
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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage
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Visualizing and Quantifying Endonuclease-Based Site-Specific DNA Damage

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Area of Science:

  • Cellular biology
  • Molecular genetics
  • DNA repair mechanisms

Background:

  • Tel2 protein is essential and conserved across eukaryotes, playing a key role in DNA damage and replication stress responses.
  • Tel2 interacts with PI3-kinase related protein kinases (PIKKs) in various organisms, and its absence destabilizes PIKKs in mammalian cells.
  • Previous studies in Saccharomyces cerevisiae demonstrated Tel2 interaction with Tel1 (yeast ATM kinase), disrupted by the tel2-1 mutation, affecting DNA damage response.

Purpose of the Study:

  • To investigate the interaction between Tel2 and Mec1 (yeast ATR kinase) in Saccharomyces cerevisiae.
  • To determine the effect of the tel2-1 mutation on the Tel2-Mec1 interaction and Mec1 function.
  • To re-evaluate the role of Tel2 in regulating PIKK stability and function.

Main Methods:

  • Yeast two-hybrid assays to study protein-protein interactions.
  • Immunoblotting to assess protein levels.
  • Fluorescence microscopy to observe protein localization at DNA damage sites.

Main Results:

  • Tel2 physically interacts with Mec1 in Saccharomyces cerevisiae.
  • The tel2-1 mutation disrupts the physical interaction between Tel2 and Mec1.
  • Despite reduced levels, Mec1 retains its ability to localize to DNA damage sites and function in signaling.

Conclusions:

  • The Tel2 protein's role extends beyond global PIKK stability regulation.
  • Tel2 exhibits specific and differential regulation of individual PIKKs, including Mec1.
  • These findings necessitate a refined model for Tel2 function in DNA damage and replication stress responses.