Indexed on: 09 Nov '16Published on: 05 Nov '16Published in: Journal of Molecular Biology
Transcription has classically been considered a potential threat to genome integrity. Collision between transcription and DNA replication machinery, and retention of DNA:RNA hybrids, may result in genome instability. On the other hand, it has been proposed that active genes repair faster and preferentially via homologous recombination. Moreover, while canonical transcription is inhibited in the proximity of DNA double-strand breaks (DSBs), a growing body of evidence supports active non-canonical transcription at DNA damage sites. Small non-coding RNAs (sncRNAs) accumulate at DSB sites in mammals and several other organisms and are involved in DNA damage signaling and repair. Furthermore, RNA binding proteins (RBPs) are recruited to DNA damage sites and participate in the DNA damage response. Here, we discuss the impact of transcription on genome stability, the role of RBPs at DNA damage sites, and the function of sncRNAs generated upon damage in the signaling and repair of DNA lesions.