The bacterial SOS response is a well-characterized regulatory network encoded by most prokaryotic bacterial species and is involved in DNA repair. In addition to nucleic acid repair, the SOS response is involved in pathogenicity, stress-induced mutagenesis, and the emergence and dissemination of antibiotic resistance. Using high-throughput sequencing technology (SOLiD RNASeq), we analyzed the Burkholderia thailandensis global SOS response to the fluoroquinolone antibiotic, ciprofloxacin (CIP), and the DNA-damaging chemical, mitomycin C (MMC). We demonstrate that a B. thailandensis recA mutant (RU0643) is ϳ4-fold more sensitive to CIP in contrast to the parental strain B. thailandensis DW503. Our RNA-Seq results show that CIP and MMC treatment (P < 0.01) resulted in the differential expression of 344 genes in B. thailandensis and 210 genes in RU0643. Several genes associated with the SOS response were induced and include lexA, uvrA, dnaE, dinB, recX, and recA. At the genomewide level, we found an overall decrease in gene expression, especially for genes involved in amino acid and carbohydrate transport and metabolism, following both CIP and MMC exposure. Interestingly, we observed the upregulation of several genes involved in bacterial motility and enhanced transcription of a B. thailandensis genomic island encoding a Siphoviridae bacteriophage designated E264. Using B. thailandensis plaque assays and PCR with B. mallei ATCC 23344 as the host, we demonstrate that CIP and MMC exposure in B. thailandensis DW503 induces the transcription and translation of viable bacteriophage in a RecA-dependent manner. This is the first report of the SOS response in Burkholderia spp. to DNA-damaging agents. We have identified both common and unique adaptive responses of B. thailandensis to chemical stress and DNA damage.
Burkholderia thailandensis is a Gram-negative motile rod commonly found in stagnant waters, soils, and rice paddies in the central and northeastern areas of Thailand (1). B. thailandensis is genetically and physiologically similar to Burkholderia pseudomallei, the etiologic agent of melioidosis (1-3). In fact, extensive chromosomal similarities exist between B. thailandensis and B. pseudomallei, with the exception of various virulence genes that are encoded by B. pseudomallei and absent in B. thailandensis (4). The most notable difference between B. thailandensis and B. pseudomallei is the ability to cause disease in animals and humans. Brett et al. reported a 50% lethal dose (LD 50 ) of Ͻ10 CFU for B. pseudomallei in a hamster model in contrast to an LD 50 of Ͼ10 6 CFU for B. thailandensis (1). Likewise, the LD 50 in BALB/c mice for B. thailandensis is Ͼ10 9 CFU compared in contrast to an ϳLD 50 of 182 CFU for B. pseudomallei (5, 6).Both Gram-negative and Gram-positive bacteria respond to environmental stresses that lead to DNA damage by the induction of the bacterial SOS response (7-9). The SOS response involves upregulation of a number of genes that are important for DNA repair and the regulation of cell divisi...