In response to DNA damage causing double strand breaks (DSBs), the recombination protein Rad52 forms discrete nuclear foci after the initiation of DNA replication and S phase entry. The goal of this project is to elucidate the mechanisms underlying the control and timing of Rad52 focus formation by addressing the dependency of DSB repair (DSBR) on DNA replication or cell cycle regulators. Additionally, a method for in vivo visualization of phosphorylation events, particularly that of histone H2A in response to DNA damage is proposed. Finally, mutations in S. cerevisiae H2A conferring sensitivity to DNA damage have been isolated. These mutations will be analyzed for their effect on both the recognition and the repair of DSBs in vivo. ? ?
| Barlow, Jacqueline H; Rothstein, Rodney (2009) Rad52 recruitment is DNA replication independent and regulated by Cdc28 and the Mec1 kinase. EMBO J 28:1121-30 |
| Barlow, Jacqueline H; Lisby, Michael; Rothstein, Rodney (2008) Differential regulation of the cellular response to DNA double-strand breaks in G1. Mol Cell 30:73-85 |
