DNA replication complexes assembled at origins of replication are intrinsically highly processive. However, their progression is often hindered by lesions in or on the DNA. There is growing evidence that RNA polymerase stalled itself at a lesion in the template strand is a major obstacle, especially in UV-irradiated cells. The data presented in this book provide information and propose model on how modulation of RNA polymerase activity might enable UV-irradiated cells lacking RuvABC to overcome obstacles caused by the stalling of RNA polymerases at UV-induced DNA lesions. The proposed model for replication restart relies on PriA protein, but does not require RecBCD and thus does not proceed via recombination and Holliday junction resolution or even via processing of a DNA end by RecBCD. However, it does require the UvrABC excision repair pathway and RecG protein. The book describes studies indicating that in rpo* cells, replication forks may run directly into lesions in DNA rather than into RNA polymerase stalled at lesions, and that this leads to direct fork rescue without recombination with the aid of SOS induction, which increases excision repair to remove lesions at other sites.