The histidine kinase NahK regulates denitrification and nitric oxide accumulation through RsmA in Pseudomonas aeruginosa

Pseudomonas aeruginosa have a versatile metabolism; they can adapt to many stressors, including limited oxygen and nutrient availability. This versatility is especially important within a biofilm where multiple microenvironments are present. As a facultative anaerobe, P. aeruginosa can survive under anaerobic conditions utilizing denitrification. This process produces nitric oxide (NO) which has been shown to result in cell elongation. However, the molecular mechanism underlying this phenotype is poorly understood. Our laboratory has previously shown that NosP is a NO-sensitive hemoprotein that works with the histidine kinase NahK to regulate biofilm formation in P. aeruginosa. In this study, we identify NahK as a novel regulator of denitrification under anaerobic conditions. Under anaerobic conditions, deletion of nahK leads to a reduction of growth coupled with reduced transcriptional expression and activity of the denitrification reductases. Furthermore, during stationary phase under anaerobic conditions, ΔnahK does not exhibit cell elongation, which is characteristic of P. aeruginosa. We determine the loss of cell elongation is due to changes in NO accumulation in ΔnahK. We further provide evidence that NahK may regulate denitrification through modification of RsmA levels.