Genome-wide fork-collapse sites in MEFs from ATR inhibition [mouse]

Transient obstruction of DNA polymerase progression activates the ATR checkpoint kinase, which suppresses fork breakage, strand resection, and RPA accumulation. Herein, we use a developed DNA break-detection assay, BrITL, to identify replication-problematic loci (RPLs) that become processed into persistent double-strand breaks across the mammalian genome from ATR inhibition. Overall design: Examination of double-strand break sites in mouse embryonic fibroblasts arising from low-dose aphidicolin treatment and ATR inhibition. Two replicates of each condition are included, in addition to one input per condition, totaling 6 samples. This includes DMSO-treated controls. Samples were deep-sequenced through Illumina HiSeq.