PARticular MARks: Histone ADP-ribosylation and the DNA damage response.

DNA Repair (Amst)

Department of Molecular Biosciences, The University of Texas at Austin, Austin, TX 78712, USA; Livestrong Cancer Institutes, Dell Medical School, The University of Texas at Austin, Austin, TX 78712, USA. Electronic address:

Published: August 2024

AI Article Synopsis

  • DNA damage triggers a complex response at the cellular and molecular levels, with histone proteins playing a key role in organizing DNA and managing the genome's integrity.
  • Histone ADP-ribosylation (ADPr) is recognized as an important modification that influences the chromatin response to DNA damage, affecting how repair factors are recruited to sites of damage.
  • Recent advancements in technology have improved our understanding of histone ADPr's role in DNA damage response, which has significant implications for human diseases, especially cancer, and opens pathways for future research on potential treatments.

Article Abstract

Cellular and molecular responses to DNA damage are highly orchestrated and dynamic, acting to preserve the maintenance and integrity of the genome. Histone proteins bind DNA and organize the genome into chromatin. Post-translational modifications of histones have been shown to play an essential role in orchestrating the chromatin response to DNA damage by regulating the DNA damage response pathway. Among the histone modifications that contribute to this intricate network, histone ADP-ribosylation (ADPr) is emerging as a pivotal component of chromatin-based DNA damage response (DDR) pathways. In this review, we survey how histone ADPr is regulated to promote the DDR and how it impacts chromatin and other histone marks. Recent advancements have revealed histone ADPr effects on chromatin structure and the regulation of DNA repair factor recruitment to DNA lesions. Additionally, we highlight advancements in technology that have enabled the identification and functional validation of histone ADPr in cells and in response to DNA damage. Given the involvement of DNA damage and epigenetic regulation in human diseases including cancer, these findings have clinical implications for histone ADPr, which are also discussed. Overall, this review covers the involvement of histone ADPr in the DDR and highlights potential future investigations aimed at identifying mechanisms governed by histone ADPr that participate in the DDR, human diseases, and their treatments.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.dnarep.2024.103711DOI Listing

Publication Analysis

Top Keywords

dna damage
28
histone adpr
24
damage response
12
dna
10
histone
10
histone adp-ribosylation
8
response dna
8
human diseases
8
damage
7
adpr
7

Similar Publications

Sperm motility is the prime functional attribute for semen quality and fertility of the bull. However, the bull's age directly affects the semen quality, and the bull's fertility and productive life decline with age. Even though research on age has been conducted in the past, it is still unclear how old a bull should be maintained at artificial insemination centers.

View Article and Find Full Text PDF

Quantifying DNA Lesions and Circulating Free DNA: Diagnostic Marker for Electropathology and Clinical Stage of AF.

JACC Clin Electrophysiol

December 2024

Physiology, Amsterdam Cardiovascular Sciences, Heart Failure, and Arrhythmias, Amsterdam University Medical Center, location Vrije Universiteit Amsterdam, Amsterdam, the Netherlands. Electronic address:

Background: Atrial fibrillation (AF) persistence is associated with molecular remodeling that fuels electrical conduction abnormalities in atrial tissue. Previous research revealed DNA damage as a molecular driver of AF.

Objectives: This study sought to explore the diagnostic value of DNA damage in atrial tissue and blood samples as an indicator of the prevalence of electrical conduction abnormalities and stage of AF.

View Article and Find Full Text PDF

Extensive homologous recombination safeguards oocyte genome integrity in mammals.

Nucleic Acids Res

January 2025

MOE Key Laboratory of Biosystems Homeostasis and Protection, College of Life Sciences, Zhejiang University, No.866 Yuhangtang Road, 310058, Hangzhou, China.

Meiosis in mammalian oocytes is interrupted by a prolonged arrest at the germinal vesicle stage, during which oocytes have to repair DNA lesions to ensure genome integrity or otherwise undergo apoptosis. The FIRRM/FLIP-FIGNL1 complex dissociates RAD51 from the joint DNA molecules in both homologous recombination (HR) and DNA replication. However, as a type of non-meiotic, non-replicative cells, whether this RAD51-dismantling mechanism regulates genome integrity in oocytes remains elusive.

View Article and Find Full Text PDF

GDBr: genomic signature interpretation tool for DNA double-strand break repair mechanisms.

Nucleic Acids Res

January 2025

Department of Convergent Bioscience and Informatics, College of Bioscience and Biotechnology, Chungnam National University, 99, Daehak-ro, Yuseong-gu, Daejeon 34134, Republic of Korea.

Large genetic variants can be generated via homologous recombination (HR), such as polymerase theta-mediated end joining (TMEJ) or single-strand annealing (SSA). Given that these HR-based mechanisms leave specific genomic signatures, we developed GDBr, a genomic signature interpretation tool for DNA double-strand break repair mechanisms using high-quality genome assemblies. We applied GDBr to a draft human pangenome reference.

View Article and Find Full Text PDF

Altered DNA dynamics at lesion sites are implicated in how DNA repair proteins sense damage within genomic DNA. Using laser temperature-jump (T-jump) spectroscopy combined with cytosine-analog Förster Resonance Energy Transfer (FRET) probes that sense local DNA conformations, we measured the intrinsic dynamics of DNA containing 3 base-pair mismatches recognized in vitro by Rad4 (yeast ortholog of XPC). Rad4/XPC recognizes diverse lesions from environmental mutagens and initiates nucleotide excision repair.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!