Next-generation DNA damage sequencing

Abstract

DNA damage sequencing strategies.

Biomarkers of nucleic acid oxidation – A summary state-of-the-art

“…However, technological advances have led to an improved approach for the detection of modified nucleobases in genomic DNA, utilizing next generation sequencing after immunoprecipitation of the damaged regions using anti-8-oxodG antibody (reviewed in Ref. [ 162 ], and considered more in “The Future” section of this review).…”

Molecular beacons with oxidized bases report on substrate specificity of DNA oxoguanine glycosylases

“…15,16 DNA glycosylases that remove these oxidized nucleobases initiate base excision repair, 13 and are key reagents for emerging DNA damage detection and sequencing technologies. 7,[17][18][19][20][21][22] Oxoguanine glycosylases have been used widely to detect DNA oxidation, including in the comet assay, 19 mass spectrometry 20 and DNA damage sequencing. 18,21,22 In the oxidation-sequencing methods click-code-seq and entrap-seq, formamidopyrimidine-DNA glycosylase (Fpg) or a human 8-oxoG glycosylase (hOGG1) K249Q mutant were used to enrich and map guanine oxidation in a yeast and mouse genome, respectively.…”

Next Generation Sequence-based Technologies for Analyzing DNA Strand Breaks

“…Genomic DNA is constantly exposed to exogenous stimuli, such as ultraviolet (UV) or gamma radiation (Takahashi et al 2019, Suto et al 2020, environmental pollution (Basu et al 2019, Hani et al 2020, artificial chemicals (Ergin et al 2020, Gantayat et al 2020, chemotherapeutic drugs (Gupta et al 2020), dietary genotoxins, and endogenous stimulants during physiological cellular processes (Jackson and Bartek 2009, Paigen and Petkov 2010, Diaz and Pecinka 2017, Tubbs and Nussenzweig 2017, Toyoda and Matsunaga 2019, Marques et al 2020, Mingard et al 2020, Nishioka et al 2020. These stimulants are known to induce approximately 70,000 lesions every day in each human cell, including single-strand breaks (SSBs) and double-strand breaks (DSBs), which are essentially fixed via various DNA repair pathways (Kunkel 2015, Tubbs andNussenzweig 2017); however, sometimes DNA damage is not repaired correctly, and the accumulation of these unrepaired damages is known to cause various pathological conditions, such as premature aging, cancer, and neurological disorders (Lord and Ashworth 2012, Baranello et al 2014, Canela et al 2016, González and Plasencia 2017.…”

“…DSBs arise in various physiological conditions such as meiosis, transcription, and replication stress, and during the repair of other types of DNA damage (Negrini et al 2010, Baudat et al 2013, Madabhushi et al 2015, Yan et al 2017, Mingard et al 2020, and it is the most profound damage among various lesions as it causes cell death, cell cycle arrest, translocations, deletions, amplification, and formation of oncogenic mutations (Bennett et al 1993, Sandell and Zakian 1993, Jackson and Bartek 2009, Zhang et al 2010a, Crosetto et al 2013). In the past two decades, several techniques have been developed for mapping genome wide DSBs.…”