RNA-seq of E. coli strain UTI89 with isogenic mutants lacking QseB and PmrA following activation with ferric iron

Antibiotic resistance is a growing global health threat. Most research has focused on understanding how mobile genetic elements are acquired by pathogenic bacteria. However, bacteria have intrinsic chromosomally encoded systems to protect themselves against antimicrobial assault. Our lab has uncovered such a system in uropathogenic E. coli. PmrAB and QseBC are connected two component systems that confer resistance to polymyxins, a last resort antibiotic. The histidine kinase PmrB responds to ferric iron and activates its cognate response regulator PmrA, as well as the non-cognate response regulator QseB. QseC, the other histidine kinase plays an important role in resetting the system. To better understand how PmrAB and QseBC mediate polymyxin resistance, this project aimed to elucidate the regulon of the two response regulators QseB and PmrA in the uropathogenic E. coli strain UTI89. In this strain, isogenic mutants were made lacking qseB and pmrA singly and together. These strains and wild-type UTI89 were stimulated with ferric iron and samples for RNA sequencing were taken prior to stimulation and at 15 and 60 minutes post stimulation. Samples were then sent for sequencing on the Illumina platform and analyzed using Rockhopper software.