Skip to main content
. 2012 Sep 16;40(21):10795–10808. doi: 10.1093/nar/gks850

Figure 6.

Figure 6.

Model for the role of Spartan in DNA damage tolerance. We suggest that at the stalled replication fork, the Rad6-Rad18-dependent PCNA ubiquitylation and the USP1-dependent PCNA deubiquitylation are dynamic processes, of which balance determines the life-time of ubiquitin-PCNA and the choice of fork rescue mechanism. In the absence of ubiquitin-PCNA, replication fork can be rescued by recombination-dependent mechanisms, which, however, have a potential for DNA rearrangements. In the presence of ubiquitin-conjugated-PCNA, damage bypass or template switching can provide replication through the lesion without the formation of a DSB intermediate. Spartan can provide one regulatory level by binding to ubiquitin-modified PCNA, which protects against PCNA deubiquitylation by USP1. Thus, Spartan can channel the reviving of stalled replication from a recombination-dependent pathway that does not require PCNA ubiquitylation to PCNA ubiquitylation-dependent translesion synthesis or PCNA polyubiquitylation-dependent template switching pathways.