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. Author manuscript; available in PMC: 2016 Apr 26.
Published in final edited form as: Biochemistry. 2016 Apr 12;55(16):2309–2318. doi: 10.1021/acs.biochem.6b00117

Figure 2.

Figure 2

Translesion synthesis (TLS) models before 1998. (A) The Bridges–Woodgate two-step model.31 In this model translesion synthesis (TLS) is catalyzed by DNA polymerase (pol) III that requires a RecA molecule for nucleotide insertion opposite a template lesion (X) and then requires the UV mutagenesis gene products UmuDC to copy past the lesion. (B) The Echols mutasome model.35 RecA nucleoprotein filament (RecA*) assembles in cis at a lesion site (X) on the template strand of DNA being copied. A multiprotein complex, including pol III holoenzyme, UmuC, and UmuD', is then recruited to the DNA allowing TLS resulting in mutations targeted opposite the lesion.