m(7)G modification in mRNA cooperates with QKI to promote homologous recombination repair.

m7G-modified RNA accumulates at DNA double-strand break sites and recruits QKI5 to selectively promote homologous recombination, enabling DNA end resection via MRE11.

• Why it matters: DSB repair pathway choice depends on DNA end resection, but how cytoplasmic m7G-modified RNA influences HR remains unclear.
• What they did: The study shows m7G-modified RNA at DSBs recruits QKI5, which directly interacts with MRE11 to enhance its DNA binding and supports MRE11-RAD50-NBS1 recruitment; QKI5 depletion reduces HR efficiency.
• The result: Higher QKI5 expression is associated with radiotherapy resistance in mouse models and clinical cohorts, suggesting the m7G RNA–QKI5–MRE11 axis regulates HR choice and QKI5 may be a therapeutic target.