UV-Induced Mutagenesis in Escherichia coli SOS Response: A Quantitative Model
Figure 2
Mechanism for Measuring Damage
When the replication fork stalls at a lesion, a RecA filament (RecA*) is formed. Each filament exists for an average time τRecA*. For low lesion densities (A), the filament disassembles before the replication fork reaches the next lesion. In contrast, an extreme scenario is depicted in (B) where the lesion density is so high that the replication fork reaches the next lesion before the first filament disassembles. In this case, more than one RecA filament can be present on the DNA for some time, and the average RecA* concentration is correspondingly higher. For intermediate lesion densities, the average concentration of RecA* also increases with the lesion density, its value being determined by the interplay between the stall time (τstalled), distance between lesions (1/μ), speed of the fork on undamaged DNA (v), and the RecA filament lifetime (τRecA*) (see main text).