DNA-Histone Cross-Links: Formation and Repair.
DNA repair
DNA-histone cross-link
chromatin
genome instability
nucleosome core particle
proteasome
spartan protease
Journal
Frontiers in cell and developmental biology
ISSN: 2296-634X
Titre abrégé: Front Cell Dev Biol
Pays: Switzerland
ID NLM: 101630250
Informations de publication
Date de publication:
2020
2020
Historique:
received:
16
09
2020
accepted:
30
11
2020
entrez:
7
1
2021
pubmed:
8
1
2021
medline:
8
1
2021
Statut:
epublish
Résumé
The nucleosome is a stretch of DNA wrapped around a histone octamer. Electrostatic interactions and hydrogen bonds between histones and DNA are vital for the stable organization of nucleosome core particles, and for the folding of chromatin into more compact structures, which regulate gene expression via controlled access to DNA. As a drawback of tight association, under genotoxic stress, DNA can accidentally cross-link to histone in a covalent manner, generating a highly toxic DNA-histone cross-link (DHC). DHC is a bulky lesion that can impede DNA transcription, replication, and repair, often with lethal consequences. The chemotherapeutic agent cisplatin, as well as ionizing and ultraviolet irradiations and endogenously occurring reactive aldehydes, generate DHCs by forming either stable or transient covalent bonds between DNA and side-chain amino groups of histone lysine residues. The mechanisms of DHC repair start to unravel, and certain common principles of DNA-protein cross-link (DPC) repair mechanisms that participate in the removal of cross-linked histones from DNA have been described. In general, DPC is removed via a two-step repair mechanism. First, cross-linked proteins are degraded by specific DPC proteases or by the proteasome, relieving steric hindrance. Second, the remaining DNA-peptide cross-links are eliminated in various DNA repair pathways. Delineating the molecular mechanisms of DHC repair would help target specific DNA repair proteins for therapeutic intervention to combat tumor resistance to chemotherapy and radiotherapy.
Identifiants
pubmed: 33409281
doi: 10.3389/fcell.2020.607045
pmc: PMC7779557
doi:
Types de publication
Journal Article
Review
Langues
eng
Pagination
607045Subventions
Organisme : NCI NIH HHS
ID : R01 CA213223
Pays : United States
Informations de copyright
Copyright © 2020 Pachva, Kisselev, Matkarimov, Saparbaev and Groisman.
Déclaration de conflit d'intérêts
AK is the founder and Chief Scientific Officer of InhiProt LLC. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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