Figure : Formation et conséquences des hybrides ARN:ADN aux cassures double-brin. Lorsqu’une cassure survient au sein d’un gène actif, cela entraîne l’arrêt de la transcription, ce qui facilite la formation d’un hybride ARN:ADN. Cet hybride participant à l’initiation de la réparation doit cependant être éliminé pour permettre une réparation fidèle et le maintien de l’intégrité du génome et la survie cellulaire.
When our DNA breaks, our cells repair it with remarkable precision. But an unexpected molecule – RNA – joins this process and forms unusual structures called RNA:DNA hybrids, where RNA “intertwines” with DNA. Gaëlle Legube, Aline Marnef, Thomas Clouaire, Florian Saur, Emma Lesage, Léa Pradel, Sarah Collins, Anne-Laure Finoux, Emile Alghoul, Benjamin Le Bozec, Vincent Rocher, Romane Carette, Nadine Puget, Marie Couralet and Mélanie Petiot (MCD-CBI) have just clarified the origin of the RNA involved in forming these hybrids, which had remained highly controversial until now.
When a double-strand break occurs within an active gene, it was already known that transcription is halted. Yet, RNA:DNA hybrid structures appear precisely at the break sites. These structures consist of an RNA molecule hybridizing with a strand of DNA. So how can RNA be present exactly where its production is supposed to be shut down?
Thanks to high-throughput sequencing techniques, Gaëlle Legube and her team discovered that these RNA:DNA hybrids are not formed from newly synthesized RNA at the break site – as several previous studies had suggested – but rather involve RNA that was already present before the break occurred.
This study offers a new perspective on the role of RNA in genome repair. It opens promising avenues for targeting these mechanisms for therapeutic purposes, particularly in the development of anticancer treatments.
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