Fig 1: Schematic representation of several infectious processes affecting the DDR.The DDR regulates DNA repair, cell-cycle checkpoints in order to halt cellular proliferation, or, if the damage is too important, cell death. Etoposide is a cytotoxic agent which causes DNA strand breaks. DNA lesions are recognized by the MRN complex (MRE11, RAD50, and NBS1) and leads to the phosphorylation of ATM and further activation of the DDR including phosphorylation of p53, CHK2, and other substrates. L. monocytogenes (Listeria), S. flexneri (Shigella), C. trachomatis (Chlamydia) all induce DNA breaks during infection but impair the DDR using different mechanisms. L. monocytogenes LLO, through pore formation induces degradation of Mre11, an associated block in the DDR, no cell cycle arrest, and no cell death (Stavru et al., 2011). S. flexneri infection leads to a decrease in the levels of p53 and cell death (Bergonioux et al., 2012), whereas C. trachomatis blocks recruitment of the MRN complex and blocks cell cycle arrest (Chumduri et al., 2013).