Pseudomonas aeruginosa causes acute and chronic human infections and is the major cause of morbidity and mortality in cystic fibrosis (CF) patients. We previously determined that the sn-glycerol-3-phosphate dehydrogenase encoded by glpD plays a larger role in P. aeruginosa physiology beyond its role in glycerol metabolism. To better understand the effect of a glpD mutation on P. aeruginosa physiology we compared the transcriptomes of P. aeruginosa strain PAO1 and the PAO1ΔglpD mutant using RNA-seq analysis. We determined that a null mutation of glpD significantly altered amino acid metabolism in P. aeruginosa and affected the production of intermediates that are channelled into the tricarboxylic acid cycle. Moreover, the loss of glpD induced a general stress response mediated by RpoS in P. aeruginosa. Several other phenotypes observed for the P. aeruginosa glpD mutant include increased persister cell formation, reduced extracellular ATP accumulation and increased heat output. Taken together, these findings implicate sn-glycerol-3-phosphate dehydrogenase as a key player in energy metabolism in P. aeruginosa.
Keywords: Pseudomonas aeruginosa; RpoS; bioenergetics; glycerol; persister cells; transcriptome.