DNA repair is essential for cell survival. In all domains of life, error-prone and error-free repair pathways ensure maintenance of genome integrity under stress. Although mutagenic, low fidelity repair mechanisms help avoid potential lethality associated with unrepaired damage, thus making them important for genome maintenance, and in some cases, the preferred mode of repair. However, cells carefully regulate pathway choice to restrict activity of these pathways to only certain conditions. One such repair mechanism is Translesion Synthesis (TLS), where a low fidelity DNA polymerase is employed to synthesize across a lesion. In bacteria, TLS is a potent source of stress-induced mutagenesis, with potential implications in cellular adaptation as well as antibiotic resistance. Extensive genetic and biochemical studies, predominantly in Escherichia coli, have established a central role for TLS in bypassing bulky DNA lesions associated with ongoing replication, either at or behind the replication fork. More recently, imaging-based approaches have been applied to understand the molecular mechanisms of TLS and how its function is regulated. Together, these studies have highlighted replication-independent roles for TLS as well. In this review, we discuss the current status of research on bacterial TLS, with emphasis on recent insights gained mostly through microscopy at the single-cell and single-molecule level.