Francesca Storici and Ailone E. Tichon
Small RNAs generated at DNA break sites are implicated in mammalian DNA repair. Now, a study shows that following the formation of DNA double-strand breaks, bidirectional transcription events adjacent to the break generate small RNAs that trigger the DNA damage response by local RNA:RNA interactions.
Maintenance of DNA integrity is crucial for a cell to have a healthy life and for transmission of accurate genetic information to its progeny. Exogenous agents, including radiation or chemicals, as well as endogenous sources, such as reactive oxygen species or defects in DNA metabolism, pose threats to genome stability. Among the most dangerous DNA lesions are DNA double-strand breaks (DSBs), which if not properly and timely sealed can become sites of mutations or chromosomal rearrangements — well-known hallmarks of cancer and other genetic disorders1. The process of DSB repair is one of the most extensively studied mechanisms of DNA repair, yet much remains to be understood about its players and dynamics.
The DNA damage response (DDR) is a complex network of cellular pathways that detect DNA lesions and organize a response signal cascade to repair the DNA. In this issue of Nature Cell Biology, Michelini et al.2 uncover an aspect of the DDR in which RNAs are the directors. The study shows that sequencespecific RNA:RNA interactions orchestrate the DDR in response to DSBs.
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News and Views pice in reference to the Walter Lab NCB paper (ref. 164 at https://sites.lsa.umich.edu/walter-lab/publications)