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Microorganisms in anaerobic Biological treatment under the nitrate nitrogen load in the EGSB

ABSTRACT: Microorganisms in anaerobic Biological treatment under the nitrate nitrogen load in the EGSB Raw sequence reads

PROVIDER: PRJNA558133 | ENA |

REPOSITORIES: ENA

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Microorganisms in anaerobic Biological treatment under the nitrate nitrogen load in the EGSB

Project description:Microorganisms in anaerobic Biological treatment under the nitrate nitrogen load in the EGSB Raw sequence reads

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Microorganisms in anaerobic biological treatment in the EGSB

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Effects of two-component system NarQ/P deletion on gene expression of Actinobacillus pleuropneumoniae in nitrate-rich anaerobic growth

Project description:Nitrate metabolism is an adaptation mechanism used by many bacteria for survival under anaerobic environments. As a by-product of inflammation, nitrate is used by the intestinal bacterial pathogens to enable gut infection. However, the responses of bacterial respiratory pathogens to nitrate are less well understood. Actinobacillus pleuropneumoniae is an important bacterial respiratory pathogen of swine. Previous studies have suggested that adaptation of A. pleuropneumoniae to anaerobiosis is important for infection. In this work, A. pleuropneumoniae growth and pathogenesis in response to the nitrate were investigated. Nitrate significantly promoted A. pleuropneumoniae growth under anaerobic condition in vitro and lethality in mice. By using narQ and narP deletion mutants, and single-residue mutation complementary strains of ΔnarQ, the two-component system NarQ/P were confirmed to be critical for nitrate induced growth, with Arg50 in NarQ as an essential functional residue. Transcriptome analysis showed that nitrate up-regulated multiple energy-generating pathways, including nitrate metabolism, mannose and pentose metabolism and glycerolipid metabolism via the regulation of NarQ/P. Furthermore, narQ, narP and its target gene encoding the nitrate reductase Nap contributed to the pathogenicity of A. pleuropneumoniae. The Nap inhibitor tungstate significantly reduced the survival of A. pleuropneumoniae in vivo, suggesting that Nap is a potential drug target. These results give new insights into how the respiratory pathogen A. pleuropneumoniae utilizes alternative electron acceptor nitrate to overcome the hypoxia microenvironment, which can occur in the inflammatory or necrotic infected tissues.

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