The nitric oxide synthase gene negatively regulates biofilm formation in .

is a clinically important conditioned pathogen that can cause a troublesome chronic implant-related infection once a biofilm is formed. The nitric oxide synthase () gene, which is responsible for endogenous nitric oxide synthesis, has already been found in the genome of ; however, the specific mechanisms associated with the effects of on pathogenicity are still unknown. The purpose of the current study was to investigate whether the gene has an impact on biofilm formation in . Bioinformatics analysis of the gene was performed, and homologous recombination was subsequently employed to delete this gene. The effects of the gene on biofilm formation of and its underlying mechanisms were analyzed by bacterial growth assays, biofilm semiquantitative determination, Triton X-100-induced autolysis assays, and bacterial biofilm dispersal assays. Additionally, the transcription levels of , , , and , which are related to biofilm formation, were further investigated by qRT-PCR following deletion. Phylogenetic analysis revealed that the gene was conserved between bacterial species originating from different genera. The deletion strain of 1457 and its counterpart were successfully constructed. Disruption of the gene resulted in significantly enhanced biofilm formation, slightly retarded bacterial growth, a markedly decreased autolysis rate, and drastically weakened bacterial biofilm dispersal. Our data showed that the , and genes were significantly upregulated, while the and genes were significantly downregulated, compared with the wild strain. Therefore, these data strongly suggested that the gene can negatively regulate biofilm formation in by affecting biofilm aggregation and dispersal.