GSE43504
Genome-wide mapping of early replication fragile sites (ERFS)
DNA double strand breaks (DSBs) in B lymphocytes are thought to arise  stochastically during replication (S phase) or as a result of targeted DNA damage by  activation induced cytidine deaminase (AID) in G1. Here we identify a novel class of  recurrent, early replicating and AID independent DNA lesions, termed early  replication fragile sites (ERFS), by genome-wide localization of DNA repair proteins  DNA double strand breaks (DSBs) in B lymphocytes are thought to arise  stochastically during replication (S phase) or as a result of targeted DNA damage by  activation induced cytidine deaminase (AID) in G1. Here we identify a novel class of  recurrent, early replicating and AID independent DNA lesions, termed early  replication fragile sites (ERFS), by genome-wide localization of DNA repair proteins  DNA double strand breaks (DSBs) in B lymphocytes are thought to arise stochastically during replication (S phase) or as a result of targeted DNA damage by activation induced cytidine deaminase (AID) in G1. Here we identify a novel class of recurrent, early replicating and AID independent DNA lesions, termed early replication fragile sites (ERFS), by genome-wide localization of DNA repair proteins  RPA, SMC5, gamma-H2AX, and BRCA1 in B cells subjected to replication stress. Overall design: Protein-DNA association for four DNA damage response proteins (RPA, SMC5, g-H2AX, BRCA1), BrdU incorporation, and gene transcription in B lymphocytes with and without hydroxyurea treatment were examined.