Related Experiment Video
Updated: Sep 30, 2025

Visualization of DNA Repair Proteins Interaction by Immunofluorescence
Published on: June 26, 2020
New insights into the DNA repair pathway choice with NuA4/TIP60
Anahita Lashgari1, Pata-Eting Kougnassoukou Tchara2, Jean-Philippe Lambert2
1St-Patrick Research Group in Basic Oncology, Canada; Laval University Cancer Research Center, CHU de Québec-Université Laval Research Center, Quebec City, QC, Canada; Department of Molecular Medicine, Big Data Research Center, Université Laval, Quebec, Canada.
Abstract:
In eukaryotic cells, DNA double-strand breaks (DSBs) can be repaired through two main pathways, non-homologous end-joining (NHEJ) or homologous recombination (HR). The selection of the repair pathway choice is governed by an antagonistic relationship between repair factors specific to each pathway, in a cell cycle-dependent manner. The molecular mechanisms of this decision implicate post-translational modifications of chromatin surrounding the break. Here, we discuss the recent advances regarding the function of the NuA4/TIP60 histone acetyltransferase/chromatin remodeling complex during DSBs repair. In particular, we emphasise the contribution of NuA4/TIP60 in repair pathway choice, in collaboration with the SAGA acetyltransferase complex, and how they regulate chromatin dynamics, modify non-histone substrates to allow DNA end resection and recombination.
Insights
The NuA4/TIP60 complex influences DNA double-strand break (DSB) repair pathway choice by regulating chromatin dynamics and modifying proteins. This chromatin remodeling is crucial for homologous recombination and DNA repair in eukaryotic cells.
Area of Science:
- Molecular Biology
- Cell Biology
- Genetics
Background:
- Eukaryotic cells repair DNA double-strand breaks (DSBs) via non-homologous end-joining (NHEJ) or homologous recombination (HR).
- Pathway selection depends on antagonistic repair factors and cell cycle status.
- Chromatin modifications around DSBs are key to this decision.
Purpose of the Study:
- To review recent advances in understanding the NuA4/TIP60 complex's role in DSB repair.
- To highlight NuA4/TIP60's contribution to DNA repair pathway choice.
- To elucidate how NuA4/TIP60 regulates chromatin dynamics and DNA end resection.
Main Methods:
- Literature review of recent advances in DNA repair research.
- Focus on the function of the NuA4/TIP60 histone acetyltransferase/chromatin remodeling complex.
- Discussion of the interplay between NuA4/TIP60, SAGA complex, and DNA repair pathways.
Main Results:
- NuA4/TIP60 plays a critical role in selecting the DNA repair pathway.
- This complex collaborates with the SAGA complex to modulate chromatin.
- NuA4/TIP60 modifies non-histone substrates, facilitating DNA end resection and recombination.
Conclusions:
- NuA4/TIP60 is a key regulator of DNA double-strand break repair pathway choice.
- Chromatin remodeling by NuA4/TIP60 is essential for homologous recombination.
- Understanding NuA4/TIP60 function provides insights into maintaining genomic stability.
More Related Videos
Related Concept Videos
Long-patch Base Excision Repair
Nucleotide Excision Repair
Overview of DNA Repair
Chemically...
Base-pairing and DNA Repair
Homologous Recombination
Fixing Double-strand Breaks

