implying that HR-mediated DSB repair may be involved in repairing re-replication-associated DSBs to maintain cell viability. Despite these observations, the exact mechanism of how DSBs are repaired during re-replication is still not clear. Suppression of re-replication plays critical roles in preventing genome instability when mutations and defects are present in the replication control pathways. However, such mechanisms may be more important for a normal cell to cope with mistakes at replication onset and/or during replication. For instance, reassembly of preRCs may occur at one or more origins at fault in a normal cell. In response to such mistakes, inhibition of re-replication immediately after DNA unwinding would limit re-replication to a minimal extent, possibly right after the synthesis of RNA/DNA primers or small stretches of DNA at origins.
Under this circumstance, checkpoint-activated repair pathways would be able to remove these limited duplicated sequences and repair re-replication-associated lesions, so that DNA lesions caused by transient loss of DNA replication control are fixed and a normal cell cycle can be restored. Checkpoint-induced
implying that HR-mediated DSB repair may be involved in repairing re-replication-associated DSBs to maintain cell viability. Despite these observations, the exact mechanism of how DSBs are repaired during re-replication is still not clear. Suppression of re-replication plays critical roles in preventing genome instability when mutations and defects are present in the replication control pathways. However, such mechanisms may be more important for a normal cell to cope with mistakes at replication onset and/or during replication. For instance, reassembly of preRCs may occur at one or more origins at fault in a normal cell. In response to such mistakes, inhibition of re-replication immediately after DNA unwinding would limit re-replication to a minimal extent, possibly right after the synthesis of RNA/DNA primers or small stretches of DNA at origins.Under this circumstance, checkpoint-activated repair pathways would be able to remove these limited duplicated sequences and repair re-replication-associated lesions, so that DNA lesions caused by transient loss of DNA replication control are fixed and a normal cell cycle can be restored. Checkpoint-induced
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