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Related Concept Videos

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...
Nucleotide Excision Repair01:38

Nucleotide Excision Repair

DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
Nucleotide Excision Repair01:08

Nucleotide Excision Repair

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Nucleotide Excision Repair01:08

Nucleotide Excision Repair

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Overview of DNA Repair02:25

Overview of DNA Repair

In order to be passed through generations, genomic DNA must be undamaged and error-free. However, every day, DNA in a cell undergoes several thousand to a million damaging events by natural causes and external factors. Ionizing radiation such as UV rays, free radicals produced during cellular respiration, and hydrolytic damage from metabolic reactions can alter the structure of DNA. Damages caused include single-base alteration, base dimerization, chain breaks, and cross-linkage.
Chemically...

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Analysis of Nonhomologous End Joining and Homologous Recombination Efficiency in HEK-293T Cells Using GFP-Based Reporter Systems
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GCN5 and TADA2B constitutively regulate XRCC1 function during DNA repair to maintain cell survival.

Keeeun Kim1, Junyoung Kim1,2, Darom Lee1,2

  • 1Institute of Medical Science, Ajou University School of Medicine, Suwon, Korea.

Cell Death and Differentiation
|July 3, 2026
PubMed
Summary

New proteins GCN5 and TADA2B regulate DNA repair localization by binding XRCC1, crucial for cell survival and preventing neurological diseases like SCAR26.

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • XRCC1 protein is central to DNA repair pathways like base excision repair (BER) and single-strand break repair (SSBR).
  • Disruptions in XRCC1 function are linked to neurological disorders, such as spinocerebellar ataxia autosomal recessive 26 (SCAR26).
  • While PARP1-mediated recruitment of XRCC1 is known, its constitutive regulation remains poorly understood.

Purpose of the Study:

  • To identify novel binding partners of XRCC1 involved in its constitutive regulation.
  • To elucidate the role of these partners in DNA repair localization and efficiency.
  • To understand how these interactions influence cellular responses to genotoxic stress and disease pathology.

Main Methods:

  • Co-immunoprecipitation assays to identify XRCC1 binding partners.
  • Western blotting and immunofluorescence to assess protein localization and DNA repair foci.
  • Cell viability assays and genotoxicity sensitivity tests following protein depletion.
  • Analysis of XRCC1 mutants, including disease-associated mutations, to study binding interactions.

Main Results:

  • GCN5 and TADA2B, components of the SAGA complex, were identified as novel XRCC1 binding partners.
  • GCN5 and TADA2B bind distinct BRCT domains of XRCC1 (BRCT I and BRCT II, respectively), independent of DNA damage.
  • Depletion of GCN5 or TADA2B impairs DNA repair, increases sensitivity to genotoxic stress, and elevates cell death.
  • GCN5/TADA2B deficiency rescues defects in specific XRCC1 mutants, indicating context-dependent roles.
  • The SCAR26 mutation disrupts TADA2B binding, with paradoxical inhibitory effects in the mutant context.

Conclusions:

  • GCN5 and TADA2B provide constitutive regulation of XRCC1 localization, essential for efficient DNA repair and cell survival.
  • These interactions establish a 'ready-for-action' model, preorganizing repair machinery before damage.
  • Dysregulation of these constitutive interactions contributes to cellular dysfunction and potentially neurological diseases like SCAR26.