DSBCapture: in situ capture and sequencing of DNA breaks

Lensing, Stefanie; Marsico, Giovanni; Hänsel‐Hertsch, Robert; Lam, Enid Y.N.; Tannahill, David; Balasubramanian, Shankar

doi:10.1038/nmeth.3960

Cited by 127 publications

(182 citation statements)

References 22 publications

(34 reference statements)

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“…In the first step, we analyzed public DSBCapture data from Lensing el at. [6], which is the most sensitive and accurate genome-wide mapping of DSBs to date (Fig. 1a).…”

Section: Double-strand Break Prediction Approachmentioning

confidence: 99%

“…We then compared previous DSB predictions with DSBs identified by BLESS experiments [3,6]. We also included in the comparison DSBCapture DSBs as the gold standard because of its higher sensitivity compared to BLESS: 84 821 DSBs were found by DSBCapture compared to 18 510 DSBs found by BLESS [6].…”

Section: Comparison With Bless Experiments and Validation Using An Indmentioning

confidence: 99%

“…We also included in the comparison DSBCapture DSBs as the gold standard because of its higher sensitivity compared to BLESS: 84 821 DSBs were found by DSBCapture compared to 18 510 DSBs found by BLESS [6]. We first looked at predicted DSB sites surrounding the two genes MYC and MAP2K3 (Fig.…”

Section: Comparison With Bless Experiments and Validation Using An Indmentioning

confidence: 99%

“…DSBs are most commonly found in cancer cells. Several high-throughput sequencing techniques have been developed for the genome-wide mapping of DSBs in situ such as BLESS [3], GUIDE-seq [4], END-seq [5], and DSBCapture [6]. One of the most recent techniques, DSBCapture, was used to map more than 80 000 endogenous DSBs at a resolution lower than 1 kb in human.…”

Section: Introductionmentioning

confidence: 99%

“…Other studies have shown that the epigenome can be predicted by combinations of DNA motifs and DNA shape [11][12][13][14]. On the other hand, DSBs and the resulting DNA repair mechanisms have been shown to be linked to epigenome marks, including H3K4me1/2/3 and chromatin accessibility [6]. Accordingly, PRDM9-mediated trimethylation of H3K4 (H3K4me3) was originally shown to play a critical role in regulating DSBs associated with meiotic recombination hotspots [15][16][17].…”

Section: Introductionmentioning

confidence: 99%

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Predicting double-strand DNA breaks using epigenome marks or DNA at kilobase resolution

Mourad

Cuvier

2017

Preprint

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Double-strand breaks (DSBs) result from the attack of both DNA strands by multiple sources, including radiation and chemicals. DSBs can cause the abnormal chromosomal rearrangements associated with cancer. Recent techniques allow the genome-wide mapping of DSBs at high resolution, enabling the comprehensive study of their origins. However, these techniques are costly and challenging. Hence, we devise a computational approach to predict DSBs using the epigenomic and chromatin context, for which public data are readily available from the ENCODE project. We achieve excellent prediction accuracy at high resolution. We identify chromatin accessibility, activity, and long-range contacts as the best predictors.

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“…In the first step, we analyzed public DSBCapture data from Lensing el at. [6], which is the most sensitive and accurate genome-wide mapping of DSBs to date (Fig. 1a).…”

Section: Double-strand Break Prediction Approachmentioning

confidence: 99%

Section: Comparison With Bless Experiments and Validation Using An Indmentioning

confidence: 99%

Section: Comparison With Bless Experiments and Validation Using An Indmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Predicting double-strand DNA breaks using epigenome marks or DNA at kilobase resolution

Mourad

Cuvier

2017

Preprint

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The age‐related decline of helicase function—how G‐quadruplex structures promote genome instability

Frobel,

Hänsel‐Hertsch

2024

FEBS Letters

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The intricate mechanisms underlying transcription‐dependent genome instability involve G‐quadruplexes (G4) and R‐loops. This perspective elucidates the potential link between these structures and genome instability in aging. The co‐occurrence of G4 DNA and RNA–DNA hybrid structures (G‐loop) underscores a complex interplay in genome regulation and instability. Here, we hypothesize that the age‐related decline of sirtuin function leads to an increase in acetylated helicases that bind to G4 DNA and RNA–DNA hybrid structures, but are less efficient in resolving them. We propose that acetylated, less active, helicases induce persistent G‐loop structures, promoting transcription‐dependent genome instability in aging.

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