Role of small non-coding RNAs in DSB repair in Arabidopsis thaliana
DNA double-strand breaks (DSB) are highly toxic lesions that must be repaired to avoid major losses of genetic materials or genome rearrangements. A number of highly conserved molecular pathways are involved in DSB repair, each resulting in different repair outcomes for a given DSB. Over the past decade, accumulating evidence has revealed the emergence of an unexpected new actor in DSB repair:…
Double-strand breaks (DSB) in DNA are extremely damaging and require repair to prevent loss of genetic material or genome rearrangements. Researchers have discovered that small non-coding RNAs, particularly RNA molecules, play a role in repairing these breaks. These small RNAs, called diRNAs, are generated at sites of DSBs in cells.
However, their exact function in repairing DNA was unknown. Scientists used a technique known as CRISPR/Cas12a to create targeted DSBs in specific areas of the Arabidopsis thaliana genome. The study found that these diRNAs are produced only at areas of active transcription and not at inactive or untranscribed regions. They did not detectably influence DSB repair using two common repair pathways - end-joining or microhomology-mediated end-joining.
Additionally, endogenous diRNAs have a minor impact on a repair process called homologous recombination-associated repair. In plants with impaired diRNA pathways, the formation of RAD51 foci, which are important for DNA repair, was only slightly reduced. The research suggests that diRNAs do not play a crucial role in the repair of DSBs directly, but may be involved in silencing damaged genes post-transcriptionally. This could help prevent transcription errors until the DNA is properly repaired.
Written by urgent.news from bioRxiv's reporting — not their text. Machine-written — may contain errors; check the original before relying on it.
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