In addition to various processes for removing lesions from the DNA, cells have developed specific mechanisms for tolerating unrepaired damage during the replication of the genome. These mechanisms are collectively called DNA damage bypass pathways. The Y family of DNA polymerases plays a key role in DNA damage bypass. Y family DNA polymerases, REV1, POLH (DNA polymerase eta), POLK (DNA polymerase kappa) and POLI (DNA polymerase iota), as well as the DNA polymerase zeta (POLZ) complex composed of REV3L and MAD2L2, are able to carry out translesion DNA synthesis (TLS) or replicative bypass of damaged bases opposite to template lesions that arrest high fidelity, highly processive replicative DNA polymerase complexes delta (POLD) and epsilon (POLE). REV1, POLH, POLK, POLI and POLZ lack 3'->5' exonuclease activity and exhibit low fidelity and weak processivity. The best established TLS mechanisms are annotated here. TLS details that require substantial experimental clarification have been omitted. For recent and past reviews of this topic, please refer to Lehmann 2000, Friedberg et al. 2001, Zhu and Zhang 2003, Takata and Wood 2009, Ulrich 2011, Saugar et al. 2014

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DDB1 , PCNA , POLD1 , POLD2 , POLE , POLE2 , POLH , REV3L , RFC1 , RFC2 , RFC3 , RFC4 , RFC5 , RPA1 , RPA2 , RPA3 , RPS27A , UBA52 , UBB , UBC , UBA7 , UBE2B , UFD1 , USP1 , VCP , TRIM25 , CUL4B , CUL4A , USP10 , UBE2L6 , ISG15 , PCLAF , RBX1 , MAD2L2 , POLD3 , POLI , RCHY1 , ZBTB32 , POLK , REV1 , DTL , POLE3 , NPLOC4 , POLE4 , RAD18 , POLD4 , SPRTN , USP43 , MIR3614 , MIR5193 ,