It is important to note that the abnormal origin ring only modestly contributes to cell viability and can be genetically uncoupled from replication fork collapse. In both cases, physical interaction with the checkpoint or checkpointdependent phosphorylation of replication or recombinationrepair enzymes has been invoked.The DNA polymerase aprimase complex phosphorylation are thought to be implicated in stabilizing the replisomefork association.The concept emerging from these results is that stalled forks do not accumulate breaks or recombinogenic intermediates unless the forks are prone to collapse, as is the case with replication checkpoint mutants and with cells that operate with an altered replication program.In this respect, it is interesting that cells experiencing slow replication due to limiting levels of DNA polymerases accumulate hotspots for recombination at specic chromosomal regions that resemble mammalian fragile sites. In addition to protecting the stalled forks from collapsing, replication checkpoints are also thought to mediate the damage response that promotes replication resumption following fork collapse.Although numerous details remain to be worked out, fork restart is also thought to be largely mediated through phosphorylation of targets and their subsequent recruitment to sites of damage.In the following section we will discuss the mechanisms implicated in restarting replication and those that might modulate the choice of the pathway responsible for processing DNA lesions during replication.Recombination mechanisms assist completion of replication when forks collapse in regions where there are no converging forks that could complete replication, or when the DNA lesions or the stalled replication forks are processed to doublestrand breaks. Unlike S phase replication, however, recombinationmediated replication does not appear to require MCM or replication initiation functions, consistent with the view that MCM loading is restricted to G, which ensures that origin ring and replication occur just once per cell cycle. Damage bypass replication mechanisms either are assisted by specialized translesion synthesis polymerases or utilize the genetic information encoded by the undamaged sister chromatid to overcome intraS damage and replication impediments.Templateswitchmediated damage bypass might be assisted by joint structures resembling hemicatenanes, in which one newly synthesized strand is coiled around the other newly synthesized strand, and which were shown to form after origin ring and to migrate chasing the forks. Recent studies have unmasked several proteins and posttranslational modication mechanisms capable of coordinating or modulating the choice of the pathway used to process DNA lesions during replication, and we will briey note them here.PCNA, a key signal integrator at the replication fork, is target for both ubiquitin and SUMO modications. Posttranslational modication of several other proteins in addition to PCNA was shown to regulate their function in the DNA damage response.RecQ helicases are also targets for checkpoint and posttranslational modications, and have been implicated in maintaining genome stability, probably through their role in the recombination events that occur in response to replication damage.Important issues, however, such as mitochondrial replication and the coordination between replication progression and recombination induction in the meiotic cycle, still await elucidation.Singlemolecule techniques are being developed to assess replication at the level of single replication forks, as opposed to whole cell populations, and should help us understand the replication response induced by DNA damage, chemotherapeutic drugs or mutations in the replication checkpoint.