FIGURE 1.

The two primary and most generalized pathways to solve chromosomal dimers generated by RecA-dependent repair or stalled replication forks. If the fork encounters a non-coding lesion (oxidative damage, pyrimidine dimer or an abasic site) depicted with a yellow star, it usually generates SSG (left path), although it can also lead to DSBs ends during repair by the RecFOR system. The pathways can also diverge on the location of the DNA lesion. If the lesion is located on the lagging strand template, the replisome will be able to bypass the lesion by blocking ‘Discontinuous DNA synthesis’ and then resume it downstream of the lesion, leaving a gap that would be repaired by the RecFOR system. On the other hand, a lesion on the leading strand template might transiently stop the replisome, cause its dissociation and then, bind further downstream to a new leading-strand primer, although these mechanisms are still under debate (Costes and Lambert, 2012; Yeeles et al., 2013). Alternatively, when the fork encounters a nick in the template strand (unrepaired SSG) or some cases of replication fork collapse, a DSB is generated (Right path). The DSBs are processed by the RecBCD complex that catalyzes the reattachment of the damaged DNA to the sister DNA duplex, forming a D-loop structure and eventual recognition by the replication-restart PriA protein that directs replisome assembly and resumption of the replication process in an origin-independent manner. However, odd numbers of crossover events generate dimer products (Yeeles and Dillingham, 2010; Azeroglu et al., 2016; Ðermić, 2015). Thus, if the resolution of the HJ occurs in the same sites, it will generate monomeric chromosome (Non-crossover products). In contrast, if the resolution takes place in different sites, it will generate chromosome dimers (Crossover products) (Carrasco et al., 2004; Ayora et al., 2011).