GSE196278
Atypical mitotic DNA synthesis sequencing (MiDAS-seq) in U2OS cells depleted for RAD51
DNA replication stress is an established driver of cancer-associated chromosomal rearrangements. Replication stress perturbs the duplication of late-replicating loci and activates a mitotic DNA repair pathway (termed MiDAS) for completion of replication. We here investigated RAD51-independent MiDAS. Overall design: MiDAS-seq on RAD51-depleted U2OS cells exposed to a low dose (0.4 µM) of APH in S-phase to induce replication stress