RNA-directed repair of DNA double-strand breaks

DNA double-strand breaks (DSBs) are among the most deleterious DNA lesions, which if unrepaired or repaired incorrectly can cause cell death or genome instability that may lead to cancer. To counteract these adverse consequences, eukaryotes have evolved a highly orchestrated mechanism to repair DSBs...

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Bibliographic Details
Published in:DNA repair 2015-08, Vol.32, p.82-85
Main Authors: Yang, Yun-Gui, Qi, Yijun
Format: Article
Language:English
Subjects:
Argonaute Proteins - genetics
Argonaute Proteins - metabolism
diRNA
DNA - chemistry
DNA - metabolism
DNA Breaks, Double-Stranded
DNA damage response
DNA Repair
Double-strand break
Gene Expression Regulation
Genomic Instability
Humans
MicroRNA
Rad51 Recombinase - genetics
Rad51 Recombinase - metabolism
Rad52 DNA Repair and Recombination Protein - genetics
Rad52 DNA Repair and Recombination Protein - metabolism
Recombination, Genetic
RNA
RNA - chemistry
RNA - genetics
RNA - metabolism
RNA Polymerase II - genetics
RNA Polymerase II - metabolism
Signal Transduction
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Summary:DNA double-strand breaks (DSBs) are among the most deleterious DNA lesions, which if unrepaired or repaired incorrectly can cause cell death or genome instability that may lead to cancer. To counteract these adverse consequences, eukaryotes have evolved a highly orchestrated mechanism to repair DSBs, namely DNA-damage-response (DDR). DDR, as defined specifically in relation to DSBs, consists of multi-layered regulatory modes including DNA damage sensors, transducers and effectors, through which DSBs are sensed and then repaired via DNAprotein interactions. Unexpectedly, recent studies have revealed a direct role of RNA in the repair of DSBs, including DSB-induced small RNA (diRNA)-directed and RNA-templated DNA repair. Here, we summarize the recent discoveries of RNA-mediated regulation of DSB repair and discuss the potential impact of these novel RNA components of the DSB repair pathway on genomic stability and plasticity.
ISSN:1568-7864
1568-7856
DOI:10.1016/j.dnarep.2015.04.017