University of Wollongong, School of Chemistry, Northfields Ave, Wollongong, NSW
Exposure to ultraviolet radiation leads to the formation of photoproducts (lesions) in DNA. In the model organism Escherichia coli, UV-induced DNA damage results in the formation of the RecA nucleoprotein filament (RecA*), which initiates the SOS response via cleavage of the LexA repressor. In E. coli, the LexA repressor modulates the transcription of gene products involved in DNA repair, damage tolerance, replication restart among others in a damage dependent manner. Whereas the SOS response is well characterized at the population level using a combination of genetic and biochemical methods, the heterogeneity in its spatio-temporal organization at the single-cell level remains poorly understood. Here, using single molecule imaging methods and fluorescently-tagged DNA-repair enzymes, we study the SOS response in live E. coli cells.