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  • Journal article
    Schreiber F, Kay S, Frankel G, Clare S, Goulding D, van de Vosse E, van Dissel JT, Strugnell R, Thwaites G, Kingsley RA, Dougan G, Baker Set al., 2015,

    The H<i>d</i>, H<i>j</i>, and H<i>z66</i> flagella variants of <i>Salmonella enterica</i> serovar Typhi modify host responses and cellular interactions

    , SCIENTIFIC REPORTS, Vol: 5, ISSN: 2045-2322
  • Journal article
    Thomas MS, Wigneshweraraj S, 2014,

    Regulation of virulence gene expression

    , VIRULENCE, Vol: 5, Pages: 832-834, ISSN: 2150-5594
  • Journal article
    Huynh M-H, Liu B, Henry M, Liew L, Matthews SJ, Carruthers VBet al., 2015,

    Structural Basis of <i>Toxoplasma gondii</i> MIC2-associated Protein Interaction with MIC2

    , JOURNAL OF BIOLOGICAL CHEMISTRY, Vol: 290, Pages: 1432-1441
  • Journal article
    Woodcock KJ, Kierdorf K, Pouchelon CA, Vivancos V, Dionne MS, Geissmann Fet al., 2015,

    Macrophage-derived upd3 Cytokine causes impaired glucose homeostasis and reduced lifespan in drosophila fed a lipid-rich diet

    , Immunity, Vol: 42, Pages: 133-144, ISSN: 1097-4180

    Long-term consumption of fatty foods is associated with obesity, macrophage activation and inflammation, metabolic imbalance, and a reduced lifespan. We took advantage of Drosophila genetics to investigate the role of macrophages and the pathway(s) that govern their response to dietary stress. Flies fed a lipid-rich diet presented with increased fat storage, systemic activation of JAK-STAT signaling, reduced insulin sensitivity, hyperglycemia, and a shorter lifespan. Drosophila macrophages produced the JAK-STAT-activating cytokine upd3, in a scavenger-receptor (crq) and JNK-dependent manner. Genetic depletion of macrophages or macrophage-specific silencing of upd3 decreased JAK-STAT activation and rescued insulin sensitivity and the lifespan of Drosophila, but did not decrease fat storage. NF-κB signaling made no contribution to the phenotype observed. These results identify an evolutionarily conserved “scavenger receptor-JNK-type 1 cytokine” cassette in macrophages, which controls glucose metabolism and reduces lifespan in Drosophila maintained on a lipid-rich diet via activation of the JAK-STAT pathway.
  • Journal article
    McEwan DG, Richter B, Claudi B, Wigge C, Wild P, Farhan H, McGourty K, Coxon FP, Franz-Wachtel M, Perdu B, Akutsu M, Habermann A, Kirchof A, Helfrich MH, Odgren PR, Van Hul W, Frangakis AS, Rajalingam K, Macek B, Holden DW, Bumann D, Dikic Iet al., 2015,

    PLEKHM1 Regulates <i>Salmonella</i>-Containing Vacuole Biogenesis and Infection

    , CELL HOST & MICROBE, Vol: 17, Pages: 58-71, ISSN: 1931-3128
  • Journal article
    Holden DW, 2015,

    Persisters unmasked

    , SCIENCE, Vol: 347, Pages: 30-32, ISSN: 0036-8075
  • Journal article
    Filloux A, 2015,

    Untitled

    , FEMS MICROBIOLOGY REVIEWS, Vol: 39, Pages: 1-1, ISSN: 0168-6445
  • Journal article
    Larrouy-Maumus G, Puzo G, 2015,

    Mycobacterial envelope lipids fingerprint from direct MALDI-TOF MS analysis of intact bacilli

    , TUBERCULOSIS, Vol: 95, Pages: 75-85, ISSN: 1472-9792
  • Book chapter
    Thurston TLM, holden DW, 2015,

    interactions between salmonella and the autophagy system

    , Autophagy, infection, and the immune response, Editors: jackson, swanson, Publisher: Wiley Blackwell, ISBN: 978-1-118-67764-3
  • Journal article
    Young JC, Clements A, Lang AE, Garnett JA, Munera D, Arbeloa A, Pearson J, Hartland EL, Matthews SJ, Mousnier A, Barry DJ, Way M, Schlosser A, Aktories K, Frankel Get al., 2014,

    The Escherichia coli effector EspJ blocks Src kinase activity via amidation and ADP ribosylation

    , Nature Communications, Vol: 5, ISSN: 2041-1723

    The hallmark of enteropathogenic Escherichia coli (EPEC) infection is the formation of actin-rich pedestal-like structures, which are generated following phosphorylation of the bacterial effector Tir by cellular Src and Abl family tyrosine kinases. This leads to recruitment of the Nck–WIP–N-WASP complex that triggers Arp2/3-dependent actin polymerization in the host cell. The same phosphorylation-mediated signalling network is also assembled downstream of the Vaccinia virus protein A36 and the phagocytic Fc-gamma receptor FcγRIIa. Here we report that the EPEC type-III secretion system effector EspJ inhibits autophosphorylation of Src and phosphorylation of the Src substrates Tir and FcγRIIa. Consistent with this, EspJ inhibits actin polymerization downstream of EPEC, Vaccinia virus and opsonized red blood cells. We identify EspJ as a unique adenosine diphosphate (ADP) ribosyltransferase that directly inhibits Src kinase by simultaneous amidation and ADP ribosylation of the conserved kinase-domain residue, Src E310, resulting in glutamine-ADP ribose.

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