Abstract
Genome instability is associated with myriad human diseases and is a well-known feature of both cancer and neurodegenerative disease. Until recently, the ability to assess DNA damage—the principal driver of genome instability—was limited to relatively imprecise methods or restricted to studying predefined genomic regions. Recently, new techniques for detecting DNA double strand breaks (DSBs) and single strand breaks (SSBs) with next-generation sequencing on a genome-wide scale with single nucleotide resolution have emerged. With these new tools, efforts are underway to define the “breakome” in normal aging and disease. Here, we compare the relative strengths and weaknesses of these technologies and their potential application to studying neurodegenerative diseases.
Highlights
Genome instability is associated with myriad human diseases and is a well-known feature of both cancer and neurodegenerative disease
In addition to apoptosis, accumulating or irreparable DNA damage may lead to cell senescence (Surova and Zhivotovsky, 2013) a phenotype that has been observed in DNA damage-laden post-mitotic neurons (Jurk et al, 2012; Fielder et al, 2017)
In contrast to the results reported with single strand breaks (SSBs)-seq and SSiNGLe (Baranello et al, 2014; Cao et al, 2019), using GLOE-seq, Sriramachandran et al found that SSBs were enriched at transcription termination sites (TTS) and underrepresented at transcription start sites (TSS)
Summary
Genome instability is associated with myriad human diseases and is a well-known feature of both cancer and neurodegenerative disease. New techniques for detecting DNA double strand breaks (DSBs) and single strand breaks (SSBs) with next-generation sequencing on a genome-wide scale with single nucleotide resolution have emerged.
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