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            <title xml:lang="en">NAD kinase promotes Staphylococcus aureus pathogenesis by supporting production of virulence factors and protective enzymes</title>
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            <funder>This work was funded by the Agence Nationale de la Recherche (grant ANR-17-CE18-0011-02) and supported by Institut Pasteur, Université Paris Cité and CNRS. The Yersinia Research Unit is member of the Laboratory of Excellence Integrative Biology of Emerging Infectious Diseases (ANR-10-LBX-62-IBEID). We are grateful for support for equipment from the French government Programme d'investissements d’avenir France BioImaging (ANR-10-INSB-04–01).</funder>
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              <p>Nicotinamide adenine dinucleotide phosphate (NADPH) is the primary electron donor for reductive reactions that are essential for the biosynthesis of major cell components in all organisms. Nicotinamide adenine dinucleotide kinase (NADK) is the only enzyme that catalyzes the synthesis of NADP(H) from NAD(H). While the enzymatic properties and physiological functions of NADK have been thoroughly studied, the role of NADK in bacterial pathogenesis remains unknown. Here, we used CRISPR interference to knock down NADK gene expression to address the role of this enzyme in Staphylococcus aureus pathogenic potential. We find that NADK inhibition drastically decreases mortality of zebrafish infected with S. aureus. Furthermore, we show that NADK promotes S. aureus survival in infected macrophages by protecting bacteria from antimicrobial defense mechanisms. Proteome-wide data analysis revealed that production of major virulence-associated factors is sustained by NADK. We demonstrate that NADK is required for expression of the quorum-sensing response regulator AgrA, which controls critical S. aureus virulence determinants. These findings support a key role for NADK in bacteria survival within innate immune cells and the host during infection.</p>
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              <org type="consortium">Authors are deeply indebted to Liliane Assairi, Sylvie Pochet and Gilles Labesse who led us into the world of NAD kinases. We are grateful to past and present members of the NADK consortium, all members of the Yersinia research unit and the French national reference center for plague and other yersiniosis, as well as Frédéric Barras and Daniel Ladant for helpful discussions and insightful comments. We thank Changlong Zhao for providing pSD1. We also wish to thank the members of the fish facility team Yohann Rolin and Noël Aimar for their excellent care of the fish.</org>
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