ABSTRACT
The SOS response functions as the central regulator of DNA repair and mutagenesis in most bacteria and stands as a paradigm of gene networks controlled by a master transcriptional regulator, LexA. We developed a single-molecule imaging approach to directly monitor the LexA repressor inside live Escherichia coli cells, demonstrating key mechanisms by which DNA-binding and degradation of LexA regulates the SOS response in vivo. Our approach revealed that self-cleavage of LexA occurs frequently during unperturbed growth and causes substantial heterogeneity in LexA abundances across cells. LexA variability underlies SOS gene expression heterogeneity and triggers spontaneous SOS pulses, which enhance bacterial survival in anticipation of stress.
Competing Interest Statement
The authors have declared no competing interest.