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  • Journal article
    Wang Z, Zhao S, Jiang S, Wang Y, Buck M, Matthews S, Liu Bet al., 2019,

    Resonance assignments of N-terminal receiver domain of sigma factor S regulator RssB from <i>Escherichia coli</i>

    , BIOMOLECULAR NMR ASSIGNMENTS, Vol: 13, Pages: 333-337, ISSN: 1874-2718
  • Journal article
    Tabib-Salazar A, Mulvenna N, Severinov K, Matthews SJ, Wigneshweraraj Set al., 2019,

    Xenogeneic regulation of the bacterial transcription machinery

    , Journal of Molecular Biology, Vol: 431, Pages: 4078-4092, ISSN: 0022-2836

    The parasitic life cycle of viruses involves the obligatory subversion of the host's macromolecular processes for efficient viral progeny production. Viruses that infect bacteria, bacteriophages (phages), are no exception and have evolved sophisticated ways to control essential biosynthetic machineries of their bacterial prey to benefit phage development. The xenogeneic regulation of bacterial cell function is a poorly understood area of bacteriology. The activity of the bacterial transcription machinery, the RNA polymerase (RNAP), is often regulated by a variety of mechanisms involving small phage-encoded proteins. In this review, we provide a brief overview of known phage proteins that interact with the bacterial RNAP and compare how two prototypical phages of Escherichia coli, T4 and T7, use small proteins to 'puppeteer' the bacterial RNAP to ensure a successful infection.
  • Journal article
    Howard SA, Filloux A, 2019,

    Bacterial Protein Secretion: Looking inside an injection system

    , eLife, Vol: 8, Pages: 1-3, ISSN: 2050-084X

    The proteins injected by bacteria into eukaryotic organisms can lead to fates as diverse as death and metamorphosis
  • Journal article
    Fillol-Salom A, Bacarizo J, Alqasmi M, Rafael Ciges-Tomas J, Martinez-Rubio R, Roszak AW, Cogdell RJ, Chen J, Marina A, Penades JRet al., 2019,

    Hijacking the hijackers: escherichia coli pathogenicity islands redirect helper phage packaging for their own benefit

    , Molecular Cell, Vol: 75, Pages: 1020-1030.e4, ISSN: 1097-2765

    Phage-inducible chromosomal islands (PICIs) represent a novel and universal class of mobile genetic elements, which have broad impact on bacterial virulence. In spite of their relevance, how the Gram-negative PICIs hijack the phage machinery for their own specific packaging and how they block phage reproduction remains to be determined. Using genetic and structural analyses, we solve the mystery here by showing that the Gram-negative PICIs encode a protein that simultaneously performs these processes. This protein, which we have named Rpp (for redirecting phage packaging), interacts with the phage terminase small subunit, forming a heterocomplex. This complex is unable to recognize the phage DNA, blocking phage packaging, but specifically binds to the PICI genome, promoting PICI packaging. Our studies reveal the mechanism of action that allows PICI dissemination in nature, introducing a new paradigm in the understanding of the biology of pathogenicity islands and therefore of bacterial pathogen evolution.
  • Journal article
    Wong JLC, Romano M, Kerry LE, Kwong H-S, Low W-W, Brett SJ, Clements A, Beis K, Frankel Get al., 2019,

    OmpK36-mediated Carbapenem resistance attenuates ST258 <i>Klebsiella pneumoniae</i> in vivo

    , NATURE COMMUNICATIONS, Vol: 10, ISSN: 2041-1723
  • Journal article
    Zeden MS, Kviatkovski I, Schuster CF, Thomas VC, Fey PD, Gründling Aet al., 2019,

    Identification of the main glutamine and glutamate transporters in<i>Staphylococcus aureus</i>and their impact on c-di-AMP production

    <jats:title>Summary</jats:title><jats:p>A<jats:italic>Staphylococcus aureus</jats:italic>strain deleted for the c-di-AMP cyclase gene<jats:italic>dacA</jats:italic>is unable to survive in rich medium unless it acquires compensatory mutations. Previously identified mutations were in<jats:italic>opuD</jats:italic>, encoding the main glycine-betaine transporter, and<jats:italic>alsT</jats:italic>, encoding a predicted amino acid transporter. Here, we show that inactivation of OpuD restores the cell size of a<jats:italic>dacA</jats:italic>mutant to near wild-type size, while inactivation of AlsT does not, suggesting two different mechanisms for the growth rescue. AlsT was identified as an efficient glutamine transporter, indicating that preventing glutamine uptake in rich medium rescues the growth of the<jats:italic>S. aureus dacA</jats:italic>mutant. In addition, GltS was identified as a glutamine transporter. By performing growth curves with WT,<jats:italic>alsT</jats:italic>and<jats:italic>gltS</jats:italic>mutant strains in defined medium supplemented with ammonium, glutamine or glutamate, we revealed that ammonium and glutamine, but not glutamate promote the growth of<jats:italic>S. aureus</jats:italic>. This suggests that besides ammonium also glutamine can serve as a nitrogen source under these conditions. Ammonium and uptake of glutamine via AlsT inhibited c-di-AMP production, while glutamate uptake had no effect. These findings provide, besides the previously reported link between potassium and osmolyte uptake, a connection between nitrogen metabolism and c-di-AMP signalling in<jats:italic>S. aureus</jats:italic>.</jats:p><jats:sec><jats:title>Graphical abstract</jats:title><jats:fig id="ufig1" position="float" fig-type="figure" orientation="portrait"><j
  • Journal article
    Valentini M, Filloux A, 2019,

    Multiple Roles of c-di-GMP Signaling in Bacterial Pathogenesis

    , Annual Review of Microbiology, Vol: 73, Pages: 387-406, ISSN: 0066-4227

    The intracellular signaling molecule cyclic di-GMP (c-di-GMP) regulates the lifestyle of bacteria and controls many key functions and mechanisms. In the case of bacterial pathogens, a wide variety of virulence lifestyle factors have been shown to be regulated by c-di-GMP. Evidence of the importance of this molecule for bacterial pathogenesis has become so great that new antimicrobial agents are tested for their capacity of targeting c-di-GMP signaling. This review summarizes the current knowledge on this topic and reveals its application for the development of new antivirulence intervention strategies.
  • Journal article
    Potron A, Vuillemenot J-B, Puja H, Triponney P, Bour M, Valot B, Amara M, Cavalie L, Bernard C, Parmeland L, Reibel F, Larrouy-Maumus G, Dortet L, Bonnin RA, Plesiat Pet al., 2019,

    <i>ISAba1</i>-dependent overexpression of <i>eptA</i> in clinical strains of <i>Acinetobacter baumannii</i> resistant to colistin

    , JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY, Vol: 74, Pages: 2544-2550, ISSN: 0305-7453
  • Journal article
    Singanayagam A, Glanville N, Cuthbertson L, Bartlett NW, Finney LJ, Turek E, Bakhsoliani E, Calderazzo MA, Trujillo-Torralbo M-B, Footitt J, James PL, Fenwick P, Kemp SV, Clarke TB, Wedzicha JA, Edwards MR, Moffatt M, Cookson WO, Mallia P, Johnston SLet al., 2019,

    Inhaled corticosteroid suppression of cathelicidin drives dysbiosis and bacterial infection in chronic obstructive pulmonary disease

    , Science Translational Medicine, Vol: 11, Pages: 1-13, ISSN: 1946-6234

    Bacterial infection commonly complicates inflammatory airway diseases such as chronic obstructive pulmonary disease (COPD). The mechanisms of increased infection susceptibility and how use of the commonly prescribed therapy inhaled corticosteroids (ICS) accentuates pneumonia risk in COPD are poorly understood. Here, using analysis of samples from patients with COPD, we show that ICS use is associated with lung microbiota disruption leading to proliferation of streptococcal genera, an effect that could be recapitulated in ICS-treated mice. To study mechanisms underlying this effect, we used cellular and mouse models of streptococcal expansion with Streptococcus pneumoniae, an important pathogen in COPD, to demonstrate that ICS impairs pulmonary clearance of bacteria through suppression of the antimicrobial peptide cathelicidin. ICS impairment of pulmonary immunity was dependent on suppression of cathelicidin because ICS had no effect on bacterial loads in mice lacking cathelicidin (Camp-/-) and exogenous cathelicidin prevented ICS-mediated expansion of streptococci within the microbiota and improved bacterial clearance. Suppression of pulmonary immunity by ICS was mediated by augmentation of the protease cathepsin D. Collectively, these data suggest a central role for cathepsin D/cathelicidin in the suppression of antibacterial host defense by ICS in COPD. Therapeutic restoration of cathelicidin to boost antibacterial immunity and beneficially modulate the lung microbiota might be an effective strategy in COPD.
  • Journal article
    Ronneau S, Helaine S, 2019,

    Clarifying the Link between Toxin-Antitoxin Modules and Bacterial Persistence

    , JOURNAL OF MOLECULAR BIOLOGY, Vol: 431, Pages: 3462-3471, ISSN: 0022-2836

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