Mammalian INO80 chromatin remodeler cooperates with FANCM to mediate DNA interstrand crosslink-induced checkpoint activation and repair

Andreev, Veselin I.; Hristova, Rumyana; Asparuhova, Mila; Danovski, Georgi; Stoynov, Stoyno; Gospodinov, Anastas

doi:10.1016/j.dnarep.2018.12.007

Cited by 5 publications

(4 citation statements)

References 74 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Some remodelers play important roles in the resolution of hard to repair lesions. The Ino80 remodeler aids in the repair of interstrand cross-links ( Nagai et al, 2008 ; Horigome et al, 2014 ; Andreev et al, 2019 ). Similarly, the ISWI remodeler is required for the repair of Artemis-dependent DSB repair in heterochromatin ( Klement et al, 2014 ).…”

Section: High-let Ir Induced Damage Repair Signaling and Early Responsementioning

confidence: 99%

Chromatin and the Cellular Response to Particle Radiation-Induced Oxidative and Clustered DNA Damage

Danforth

Provencher

Goodarzi

2022

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

Exposure to environmental ionizing radiation is prevalent, with greatest lifetime doses typically from high Linear Energy Transfer (high-LET) alpha particles via the radioactive decay of radon gas in indoor air. Particle radiation is highly genotoxic, inducing DNA damage including oxidative base lesions and DNA double strand breaks. Due to the ionization density of high-LET radiation, the consequent damage is highly clustered wherein ≥2 distinct DNA lesions occur within 1–2 helical turns of one another. These multiply-damaged sites are difficult for eukaryotic cells to resolve either quickly or accurately, resulting in the persistence of DNA damage and/or the accumulation of mutations at a greater rate per absorbed dose, relative to lower LET radiation types. The proximity of the same and different types of DNA lesions to one another is challenging for DNA repair processes, with diverse pathways often confounding or interplaying with one another in complex ways. In this context, understanding the state of the higher order chromatin compaction and arrangements is essential, as it influences the density of damage produced by high-LET radiation and regulates the recruitment and activity of DNA repair factors. This review will summarize the latest research exploring the processes by which clustered DNA damage sites are induced, detected, and repaired in the context of chromatin.

show abstract

Section: High-let Ir Induced Damage Repair Signaling and Early Responsementioning

confidence: 99%

Chromatin and the Cellular Response to Particle Radiation-Induced Oxidative and Clustered DNA Damage

Danforth

Provencher

Goodarzi

2022

Front. Cell Dev. Biol.

View full text Add to dashboard Cite

show abstract

“…The INO80 remodeler consists of 10–15 polypeptides and exhibits ATP-dependent chromatin remodelling activity [ 64 ]. Besides its role in DSB repair [ 65 ] and possibly interstrand crosslink repair [ 66 ], the INO80 complex is also implicated in GG-NER [ 67 ]. Both the INO80 and the ARP5 subunits were shown to associate with and stimulate the removal of UV-induced DNA lesions.…”

Section: Chromatin Remodelling During the Dna Damage-recognition Step In Gg-nermentioning

confidence: 99%

Nucleotide excision repair leaves a mark on chromatin: DNA damage detection in nucleosomes

Apelt

Lans

Schärer

et al. 2021

Cell. Mol. Life Sci.

View full text Add to dashboard Cite

Global genome nucleotide excision repair (GG-NER) eliminates a broad spectrum of DNA lesions from genomic DNA. Genomic DNA is tightly wrapped around histones creating a barrier for DNA repair proteins to access DNA lesions buried in nucleosomal DNA. The DNA-damage sensors XPC and DDB2 recognize DNA lesions in nucleosomal DNA and initiate repair. The emerging view is that a tight interplay between XPC and DDB2 is regulated by post-translational modifications on the damage sensors themselves as well as on chromatin containing DNA lesions. The choreography between XPC and DDB2, their interconnection with post-translational modifications such as ubiquitylation, SUMOylation, methylation, poly(ADP-ribos)ylation, acetylation, and the functional links with chromatin remodelling activities regulate not only the initial recognition of DNA lesions in nucleosomes, but also the downstream recruitment and necessary displacement of GG-NER factors as repair progresses. In this review, we highlight how nucleotide excision repair leaves a mark on chromatin to enable DNA damage detection in nucleosomes.

show abstract

“…Knockdown of TIP60 in fibroblasts sensitized the cells to the ICL-inducing agent MMC, indicating a potential role in ICL repair. The ATPase INO80 was also associated with ICL repair, as INO80-deficient cells are sensitive to MMC treatment 209 . The authors also found that INO80 directly interacted with FANCM, suggesting a possible relationship between INO80 and the FA pathway 209 .…”

Section: Chromatin Remodeling During Dna Damage Repairmentioning

confidence: 99%

“…The ATPase INO80 was also associated with ICL repair, as INO80-deficient cells are sensitive to MMC treatment 209 . The authors also found that INO80 directly interacted with FANCM, suggesting a possible relationship between INO80 and the FA pathway 209 . However, there is currently no direct evidence that these remodelers affect the chromatin during ICL repair, therefore more investigations are necessary to identify which chromatin remodelers act in the FA pathway, how they interact with FA proteins, and how they affect ICL repair.…”

Section: Chromatin Remodeling During Dna Damage Repairmentioning

confidence: 99%

Beyond the Fanconi anemia pathway: new mechanisms of DNA interstrand crosslink repair

Bolner¹

View full text Add to dashboard Cite

Base mismatches Copy Number Variations DNA LESION DNA REPAIR PATHWAY Nucleotide Excision Repair Base Excision Repair ICL Repair DSB Repair Mismatch Repair Figure 1: Genome maintenance pathways The genome is challenged constantly by a wide range of endogenous and exogenous DNA damaging agents. Many types of DNA lesions exist, such as abasic sites, bulky adducts, DNA strand breaks, base mismatches, and interstrand crosslinks. To avoid genome instability, five main DNA repair pathways exist: nucleotide excision repair, base excision repair, double strand break repair, mismatch repair, and DNA interstrand crosslink repair. 22 Chapter 1 Interstrand Crosslink RepairDNA-interstrand crosslinks (ICLs) are DNA lesions that covalently bind the two strands of the double helix 76 . Because ICLs block strand separation, which is required for DNA replication and transcription, they are among the most toxic DNA lesions. ICL-inducing agents are effective in chemotherapy because they preferentially affect rapidly-dividing cells, such as cancer cells 77 . ICL inducing agents Exogenous sources of ICLsMany drugs used for chemotherapy induce ICLs, such as cisplatin and its derivatives, mitomycin C (MMC), deoxybutane (DEB), psoralens, and nitrogen mustards. These agents cause a multitude of DNA adducts, and ICLs represent just a small percentage of the lesions formed 78 . Yet, ICLs are considered the main cause of toxicity of these drugs. Although all ICLs are formed by crosslinking the two strands of the DNA, the chemical and structural properties of the various ICLs differ widely. First, the sequence context in which an ICL can form depends on the chemistry of the ICLinducing agent. For example, cisplatin and MMC induce ICLs in a 5' CG context, while psoralens act in a 5' TA sequence 78 . Secondly, the structure of the ICL and the resulting distortion of the DNA double helix differs depending on the ICL-inducing agent (Figure 5). Cisplatin causes a major distortion of the double helix, forcing the bases opposite the crosslinked Gs to be extrahelical. On the other hand, MMC, psoralens, and nitrogen mustards cause minor distortions in the DNA structure 78 . Endogenous sources of ICLsStudying ICLs formed endogenously in cells is challenging due to the scarcity of these lesions and the lack of detection methods. However, both in vivo and in vitro studies identified aldehydes as a possible endogenous source of ICLs. Aldehydes are a highly reactive class of endogenous metabolites that can form a variety of DNA adducts, including ICLs 79 (Figure 5). Acetaldehyde is a product of ethanol oxidation and the metabolism of carbohydrates, and can form ICLs between guanines 80,81 . Formaldehyde is an aldehyde that is highly concentrated in human plasma and is formed during various cellular processes such as dealkylation of methylated DNA and histone demethylation [81][82][83] . Other ICL-inducing aldehydes are generated through lipid peroxidation, such as acrolein, malondialdehyde, crotonaldehyde, and 4-hydroxynonenal 84 .In chapter 2 we show that ...

show abstract

Mammalian INO80 chromatin remodeler cooperates with FANCM to mediate DNA interstrand crosslink-induced checkpoint activation and repair

Cited by 5 publications

References 74 publications

Chromatin and the Cellular Response to Particle Radiation-Induced Oxidative and Clustered DNA Damage

Chromatin and the Cellular Response to Particle Radiation-Induced Oxidative and Clustered DNA Damage

Nucleotide excision repair leaves a mark on chromatin: DNA damage detection in nucleosomes

Beyond the Fanconi anemia pathway: new mechanisms of DNA interstrand crosslink repair

Contact Info

Product

Resources

About