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. Author manuscript; available in PMC: 2020 May 4.
Published in final edited form as: Biochim Biophys Acta Mol Basis Dis. 2019 Apr 4;1866(4):165444. doi: 10.1016/j.bbadis.2019.03.017

Fig. 3.

Fig. 3.

Different DNA repair mechanisms. A) Inter-strand cross links during replication is repaired by Fanconi anemia (FA) pathway. Cross links induced stalled forks are recognized by FANCM-FAAP23-MHF ½ complex which then recruits FA core complex with E3 ligase activity that mono-ubiquitinates FANCD2 and FANCI. Mono-ubiquitination of FANCD2 and FANCI facilitates their localization to the damaged site, which in turn recruits nucleases (XPF, MUS81, and SLX1) to remove the cross link that results in DSB. DSB is then finally fixed by homologues repair. B) Unrepaired damages are sometimes bypassed by translesion synthesis during replication to avoid stalled forks. Upon experiencing adducts during replication, RAD6/RAD18 ubiquitin complex is recruited to the stalled fork site, which mono-ubiquitinates PCNA. Mono-ubiquitinated PCNA then undergoes confirmation change that facilitates the recruitment of low fidelity polymerase eta, which bypasses the damaged DNA. After bypassing, normal high fidelity DNA polymerase replaces the polymerase eta to continue replication.