FIGURE 7.

A proposed model for the function of Hjc-S34 phosphorylation in DNA repair (stalled replication fork). DNA replication fork is usually blocked by a lesion. The stalled replication fork would be reversed to a HJ DNA by proteins such as Hjm and/or PINA (PIN domain-containing ATPase), followed by the recruitment of Hjc (Zhai et al., 2018). Phosphorylation states of Hjc might control different repair pathways: Non-phosphorylated Hjc would cleave the HJ forming a DSB which would be repaired by HR; phosphorylated Hjc at S34 would not cleave the HJ and the lesion might be repaired by mismatch repair (MMR) or base excision repair (BER). The latter may occur in the presence of high amounts of DNA lesion when treated with higher dose of DNA damaging agents. It is also possible that the choice for different pathways depended on cell cycles where S/G2 phases contain two copies of genomes for HR. MMR is probably mediated by a newly identified nuclease EndoMS, resulting in formation of a DSB repaired by HR. The replication fork might be remodeled after the lesion was removed by BER.