Final answer:
In E. coli, translesion synthesis is performed by DNA pol IV (DinB) and DNA pol V (UmuD'C). These specialized polymerases allow replication past lesions such as thymidine dimers when other repair mechanisms fail.
Step-by-step explanation:
Translesion Synthesis in E. coli
Translesion synthesis (TLS) in E. coli is a DNA damage tolerance process that allows the DNA replication machinery to replicate past a lesion, such as a thymidine dimer, on the DNA template strand. Thymidine dimers are primarily caused by ultraviolet light and result in a distortion of the DNA strand that can block replication. During SOS repair, which is an induced response to extensive DNA damage, E. coli employs specialized DNA polymerases that can replicate past these lesions.
In E. coli, DNA polymerase III is the primary enzyme required for normal DNA replication, but it is unable to bypass lesions such as thymidine dimers. However, E. coli also possesses additional polymerases, specifically DNA pol IV (DinB) and DNA pol V (UmuD'C), which are capable of translesion synthesis. These polymerases can insert nucleotides opposite the lesion, allowing replication to continue despite the presence of DNA damage. Although this process can be error-prone, it is critical for the survival of the cell under genotoxic stress, as it provides a mechanism to bypass lesions that are not repaired before the replication fork encounters them.
DNA pol IV and DNA pol V have been identified as the TLS polymerases involved in SOS repair in E. coli. While their activity is essential for cell survival in response to severe DNA damage, their fidelity is not as high as DNA pol III, leading to a higher rate of mutation during the process of lesion bypass.
In summary, the two E. coli polymerases used in translesion replication are DNA pol IV (DinB) and DNA pol V (UmuD'C). These enzymes facilitate the continuation of DNA replication past DNA lesions such as thymidine dimers when the standard repair mechanisms, like nucleotide excision repair, have not corrected the damage before the replication fork is reached.