p53-dependent chromatin relaxation is required for DNA double-strand break repair

• p53 is rapidly recruited to DNA double-strand break sites and surrounding chromatin, where it promotes chromatin relaxation to enhance DSB repair efficiency. • This novel function of p53 in DSB repair is independent of its canonical role as a transcriptional regulator, representing a paradigm shift in understanding p53's DNA damage response. • The study demonstrates that p53's direct involvement in chromatin remodeling extends beyond nucleotide excision repair to double-strand break repair, highlighting its broader role in genome stability. • These findings suggest potential therapeutic targets for enhancing DNA repair in cancer cells by modulating p53-dependent chromatin relaxation.