High-throughput 3-prime end RNA-seq of Pseudomonas aeruginosa response to Azithromycin
P. aeruginosa produces serious chronic infections in hospitalized patients and immunocompromised individuals, including cystic fibrosis patients. The molecular mechanisms by which P. aeruginosa responds to antibiotics and other stresses to promote persistent infections may provide new avenues for therapeutic intervention. Azithromycin (AZM), an antibiotic frequently utilized in cystic fibrosis treatment, is thought to improve clinical outcomes through a number of mechanisms including impaired biofilm growth and quorum sensing in P. aeruginosa. However, the mechanisms underlying the transcriptional response to AZM remain unclear. Here, we interrogated the P. aeruginosa transcriptional response to AZM using a fast and affordable genome-wide approach to quantitate RNA 3-prime-ends (3pMap). We identify new riboregulators and identify a prominent role of transcription termination in the response to AZM treatment.