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Review
. 2019 Sep 27;10:1155.
doi: 10.3389/fpls.2019.01155. eCollection 2019.

The Role of Noncoding RNAs in Double-Strand Break Repair

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Free PMC article
Review

The Role of Noncoding RNAs in Double-Strand Break Repair

Nathalie Durut et al. Front Plant Sci. .
Free PMC article

Abstract

Genome stability is constantly threatened by DNA lesions generated by different environmental factors as well as endogenous processes. If not properly and timely repaired, damaged DNA can lead to mutations or chromosomal rearrangements, well-known reasons for genetic diseases or cancer in mammals, or growth abnormalities and/or sterility in plants. To prevent deleterious consequences of DNA damage, a sophisticated system termed DNA damage response (DDR) detects DNA lesions and initiates DNA repair processes. In addition to many well-studied canonical proteins involved in this process, noncoding RNA (ncRNA) molecules have recently been discovered as important regulators of the DDR pathway, extending the broad functional repertoire of ncRNAs to the maintenance of genome stability. These ncRNAs are mainly connected with double-strand breaks (DSBs), the most dangerous type of DNA lesions. The possibility to intentionally generate site-specific DSBs in the genome with endonucleases constitutes a powerful tool to study, in vivo, how DSBs are processed and how ncRNAs participate in this crucial event. In this review, we will summarize studies reporting the different roles of ncRNAs in DSB repair and discuss how genome editing approaches, especially CRISPR/Cas systems, can assist DNA repair studies. We will summarize knowledge concerning the functional significance of ncRNAs in DNA repair and their contribution to genome stability and integrity, with a focus on plants.

Keywords: CRISPR/Cas; DNA repair; double-strand break; noncoding RNAs; plants.

Figures

Figure 1
Figure 1
The different potential roles of noncoding RNAs in DNA repair. Noncoding RNAs (in blue) can (A) guide proteins to specific sites in the genome, (B) potentially hold broken ends together (connector), (C) mediate DNA-DNA or DNA-protein interactions (anchor), (D) serve as an indicator (signal) of DNA damage, (E) provide a repair scaffold, (F) keep interfering components away (decoy), (G) recruit repair proteins (aid delivery), or (H) initiate chromatin reconstruction (remodeler).
Figure 2
Figure 2
Applications of CRISPR/Cas to study the role of noncoding RNAs. (A) Catalytically active Cas proteins (black) together with guide RNAs (blue A) can induce double- or single-strand lesions or base editing on DNA (black lines) or RNA (blue lines). (B) Nuclease-dead versions of deadCas proteins (dCas) (gray) fused with fluorescent tags or immuno-epitopes can help to visualize specific targets. (C) Fusions with activating or repressing domains or with chromatin-modifying enzymes can change gene expression. (D) Coupling interactive proteins to dCas can assemble additional proteins at the binding site, while binding specificity can be exploited to isolate proteins associated with the site.

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