The opportunistic bacterial pathogen causes acute and chronic infections that are notoriously difficult to treat. In people with cystic fibrosis, can cause lifelong lung infections, and isolation of mucoid , resulting from the overproduction of alginate, is associated with chronic infection. The histone-like protein AlgP has previously been implicated in the control of alginate gene expression in mucoid strains, but this regulation is unclear. To explore AlgP in further detail, we deleted in mucoid strains and demonstrated that the deletion of did not result in a nonmucoid phenotype or a decrease in alginate production. We showed that the promoter is expressed by both the nonmucoid strain PAO1 and the isogenic mucoid strain PDO300, suggesting that there may be genes that are differentially regulated between these strains. In support of this, using RNA sequencing, we identified a small AlgP regulon that has no significant overlap between PAO1 and PDO300 and established that alginate genes were not differentially regulated by the deletion of . Of note, we found that deleting in PAO1 increased expression of the nitric oxide operon and the nitrous oxide reductase genes and subsequently promoted growth of PAO1 under anaerobic conditions. Altogether, we have defined a narrow regulon of genes controlled by AlgP and provided evidence that alginate production is not greatly affected by AlgP, countering the long-standing premise in the field.