Genome-wide fork-collapse sites in MEFs from ATR inhibition

Transient obstruction of DNA polymerase progression activates the ATR checkpoint kinase, which suppresses fork breakage, strand resection, and RPA accumulation. Herein, we use RPA ChIP-Seq to identify replication-problematic loci (RPLs) across the mammalian genome from ATR inhibition. Examination of RPA-enriched sites in mouse embryonic fibroblasts arising from low-dose aphidicolin treatment or TIMELESS supression and ATR inhibition. Two replicates of each condition are included (except for ATRi+APH,18h, which has 3 replicates), totaling 21 samples. This includes DMSO-treated controls. Samples were deep sequenced through Illumina HiSeq.