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Updated: Aug 22, 2026
Characterizing DNA Repair Processes at Transient and Long-lasting Double-strand DNA Breaks by Immunofluorescence Microscopy
Published on: June 8, 2018
Functional links between transcription, DNA repair and apoptosis
P Berardi1, M Russell, A El-Osta
1Department of Biochemistry and Molecular Biology and Oncology, Southern Alberta Cancer Research Centre, University of Calgary, 3330 Hospital Drive N.W., Heritage Medical Research Building, T2N 4N1, Calgary, Alberta, Canada.
Abstract:
DNA damage initiates damage response pathways, cell cycle arrest and apoptosis. These processes act in a concerted fashion and remain functionally linked through mechanisms not completely understood. Programmed cell death, referred to as apoptosis, is a tightly regulated phenomenon ensuring that cells that accumulate irreversible DNA damage do not replicate. Interestingly, hyperacetylation of histone proteins, which alters transcription patterns and appears linked to DNA repair, also induces apoptosis, suggesting that aspects of chromatin modification link these very distinct processes. Modulating chromatin structure in the absence of any DNA lesions also activates key DNA damage-signalling proteins, further supporting the role of higher-order chromatin structure in mediating stress responses. This review will present an overview of the epigenetic control of eukaryotic genomes by chromatin remodelling as it pertains to DNA damage and highlight the potential role of the ING PHD proteins in linking apoptosis and DNA repair to gene transcription.
Insights
DNA damage triggers repair and apoptosis pathways. Chromatin modifications, like histone hyperacetylation, link DNA repair, gene transcription, and programmed cell death, revealing epigenetic control over stress responses.
Area of Science:
- Epigenetics
- Molecular Biology
- Cellular Biology
Background:
- DNA damage response pathways, cell cycle arrest, and apoptosis are crucial for cell survival.
- The precise mechanisms linking these processes, particularly through chromatin, are not fully understood.
- Apoptosis prevents replication of cells with irreversible DNA damage.
Purpose of the Study:
- To review the epigenetic control of eukaryotic genomes via chromatin remodeling in response to DNA damage.
- To highlight the role of ING PHD proteins in connecting apoptosis, DNA repair, and gene transcription.
Main Methods:
- Literature review of epigenetic mechanisms and DNA damage response pathways.
- Analysis of studies on chromatin modification, histone acetylation, and apoptosis.
- Examination of the function of ING PHD proteins in cellular stress responses.
Main Results:
- Histone hyperacetylation, independent of DNA lesions, can induce apoptosis and activate DNA damage signaling.
- Chromatin structure plays a significant role in mediating cellular stress responses.
- Epigenetic modifications appear to functionally link DNA repair, gene transcription, and apoptosis.
Conclusions:
- Chromatin remodeling is a key epigenetic mechanism involved in DNA damage response.
- ING PHD proteins may serve as a crucial link between DNA repair, apoptosis, and transcriptional regulation.
- Understanding these links is vital for comprehending cellular stress responses and potential therapeutic strategies.
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