Global gene expression profiling of L. interrogans serovar Copenhageni in response to UV-C irradiation. Leptospira interrogans serovar Copenhageni str. Fiocruz L1-130

The pathogen L. interrogans serovar Copenhageni can be shed in the urine of carrier mammals, and infect humans after weeks on water or mud. This wide range of possible niches implies the bacterium can be exposed to several different genotoxic stresses during its lifecycle. We assessed the impact of DNA damage in this leptospire, integrating high throughput data from ChIP-seq and DNA microarrays to determine the role of the SOS regulator LexA1. We observed 24 LexA1 binding sites located throughout the chromosome 1 and one in chromosome 2. Analyses of LexA1 ChIP-seq peak sequences revealed the SOS box is an imperfect asymmetric palindrome of 16bp, CTAA[A/T/G]CANNTG[T/A]TTAG. DNA damage caused significant changes of several aspects of bacterial physiology, decreasing expression of genes involved in energy metabolism and translation, in addition to genes related to virulence and motility. On the other hand, post replicative and recombination repair, but not the canonical DNA repair genes, were up regulated. The most striking feature of this response was the massive up-regulation of two prophages. Our findings point to an expression profile shift from cell growth and virulence to mutagenesis and recombination, emphasizing the fundamental role of DNA damage response as a highway for adaptation and evolution. Overall design: Cultures of exponential growing cells were irradiated or not with 5 J/m² UV-C and harvested after 12h. RNA isolation was performed by RNEasy mini kit from Qiagen, and cDNA synthesis and labeling with Fairplay III from Agilent. Four biological replicates were hybridized in custom slides of 8x15K from Agilent.