Publications
2014
Bonnay François, Nguyen Xuan-Hung, Cohen-Berros Eva, Troxler Laurent, Batsche Eric, Camonis Jacques, Takeuchi Osamu, Reichhart Jean-Marc, Matt Nicolas
Akirin specifies NF-κB selectivity of Drosophila innate immune response via chromatin remodeling Journal Article
In: EMBO J., vol. 33, no. 20, pp. 2349–2362, 2014, ISSN: 1460-2075.
Abstract | Links | BibTeX | Tags: Animals, bioinformatic, Cell Cycle Proteins, Chromatin Assembly and Disassembly, chromatin remodeling, DNA-Binding Proteins, Female, Genetic, Immunity, Innate, Innate immune response, M3i, Male, matt, Mutation, NF-kappa B, NF‐κB, Promoter Regions, proteomics, reichhart, Trans-Activators, Transcription Factors, Transcriptional Activation, Two-Hybrid System Techniques
@article{bonnay_akirin_2014,
title = {Akirin specifies NF-κB selectivity of Drosophila innate immune response via chromatin remodeling},
author = {François Bonnay and Xuan-Hung Nguyen and Eva Cohen-Berros and Laurent Troxler and Eric Batsche and Jacques Camonis and Osamu Takeuchi and Jean-Marc Reichhart and Nicolas Matt},
doi = {10.15252/embj.201488456},
issn = {1460-2075},
year = {2014},
date = {2014-10-01},
journal = {EMBO J.},
volume = {33},
number = {20},
pages = {2349--2362},
abstract = {The network of NF-κB-dependent transcription that activates both pro- and anti-inflammatory genes in mammals is still unclear. As NF-κB factors are evolutionarily conserved, we used Drosophila to understand this network. The NF-κB transcription factor Relish activates effector gene expression following Gram-negative bacterial immune challenge. Here, we show, using a genome-wide approach, that the conserved nuclear protein Akirin is a NF-κB co-factor required for the activation of a subset of Relish-dependent genes correlating with the presence of H3K4ac epigenetic marks. A large-scale unbiased proteomic analysis revealed that Akirin orchestrates NF-κB transcriptional selectivity through the recruitment of the Osa-containing-SWI/SNF-like Brahma complex (BAP). Immune challenge in Drosophila shows that Akirin is required for the transcription of a subset of effector genes, but dispensable for the transcription of genes that are negative regulators of the innate immune response. Therefore, Akirins act as molecular selectors specifying the choice between subsets of NF-κB target genes. The discovery of this mechanism, conserved in mammals, paves the way for the establishment of more specific and less toxic anti-inflammatory drugs targeting pro-inflammatory genes.},
keywords = {Animals, bioinformatic, Cell Cycle Proteins, Chromatin Assembly and Disassembly, chromatin remodeling, DNA-Binding Proteins, Female, Genetic, Immunity, Innate, Innate immune response, M3i, Male, matt, Mutation, NF-kappa B, NF‐κB, Promoter Regions, proteomics, reichhart, Trans-Activators, Transcription Factors, Transcriptional Activation, Two-Hybrid System Techniques},
pubstate = {published},
tppubtype = {article}
}
2011
Limmer Stefanie, Haller Samantha, Drenkard Eliana, Lee Janice, Yu Shen, Kocks Christine, Ausubel Frederick M, Ferrandon Dominique
Pseudomonas aeruginosa RhlR is required to neutralize the cellular immune response in a Drosophila melanogaster oral infection model Journal Article
In: Proc. Natl. Acad. Sci. U.S.A., vol. 108, no. 42, pp. 17378–17383, 2011, ISSN: 1091-6490.
Abstract | Links | BibTeX | Tags: Animal, Animals, Bacteremia, Bacterial Proteins, Cellular, Disease Models, ferrandon, Genes, Genetically Modified, Hemolymph, Host-Pathogen Interactions, Immunity, Insect, M3i, Mutation, Oral, Pseudomonas aeruginosa, Pseudomonas Infections, Quorum Sensing, Trans-Activators, Viral, Virulence
@article{limmer_pseudomonas_2011b,
title = {Pseudomonas aeruginosa RhlR is required to neutralize the cellular immune response in a Drosophila melanogaster oral infection model},
author = {Stefanie Limmer and Samantha Haller and Eliana Drenkard and Janice Lee and Shen Yu and Christine Kocks and Frederick M Ausubel and Dominique Ferrandon},
doi = {10.1073/pnas.1114907108},
issn = {1091-6490},
year = {2011},
date = {2011-10-01},
journal = {Proc. Natl. Acad. Sci. U.S.A.},
volume = {108},
number = {42},
pages = {17378--17383},
abstract = {An in-depth mechanistic understanding of microbial infection necessitates a molecular dissection of host-pathogen relationships. Both Drosophila melanogaster and Pseudomonas aeruginosa have been intensively studied. Here, we analyze the infection of D. melanogaster by P. aeruginosa by using mutants in both host and pathogen. We show that orally ingested P. aeruginosa crosses the intestinal barrier and then proliferates in the hemolymph, thereby causing the infected flies to die of bacteremia. Host defenses against ingested P. aeruginosa included an immune deficiency (IMD) response in the intestinal epithelium, systemic Toll and IMD pathway responses, and a cellular immune response controlling bacteria in the hemocoel. Although the observed cellular and intestinal immune responses appeared to act throughout the course of the infection, there was a late onset of the systemic IMD and Toll responses. In this oral infection model, P. aeruginosa PA14 did not require its type III secretion system or other well-studied virulence factors such as the two-component response regulator GacA or the protease AprA for virulence. In contrast, the quorum-sensing transcription factor RhlR, but surprisingly not LasR, played a key role in counteracting the cellular immune response against PA14, possibly at an early stage when only a few bacteria are present in the hemocoel. These results illustrate the power of studying infection from the dual perspective of host and pathogen by revealing that RhlR plays a more complex role during pathogenesis than previously appreciated.},
keywords = {Animal, Animals, Bacteremia, Bacterial Proteins, Cellular, Disease Models, ferrandon, Genes, Genetically Modified, Hemolymph, Host-Pathogen Interactions, Immunity, Insect, M3i, Mutation, Oral, Pseudomonas aeruginosa, Pseudomonas Infections, Quorum Sensing, Trans-Activators, Viral, Virulence},
pubstate = {published},
tppubtype = {article}
}
2008
Goulev Youlian, Fauny Jean Daniel, Gonzalez-Marti Beatriz, Flagiello Domenico, Silber Joël, Zider Alain
SCALLOPED interacts with YORKIE, the nuclear effector of the hippo tumor-suppressor pathway in Drosophila Journal Article
In: Current Biology: CB, vol. 18, no. 6, pp. 435–441, 2008, ISSN: 0960-9822.
Abstract | Links | BibTeX | Tags: Animals, Cell Proliferation, Drosophila, Drosophila Proteins, HeLa Cells, Humans, I2CT, Imagerie, Intracellular Signaling Peptides and Proteins, Morphogenesis, Nuclear Proteins, Protein Kinases, Protein-Serine-Threonine Kinases, Signal Transduction, Trans-Activators, Transcription Factors, Tumor Suppressor Proteins, Wing
@article{goulev_scalloped_2008,
title = {SCALLOPED interacts with YORKIE, the nuclear effector of the hippo tumor-suppressor pathway in Drosophila},
author = {Youlian Goulev and Jean Daniel Fauny and Beatriz Gonzalez-Marti and Domenico Flagiello and Joël Silber and Alain Zider},
url = {http://www.ncbi.nlm.nih.gov/pubmed/18313299},
doi = {10.1016/j.cub.2008.02.034},
issn = {0960-9822},
year = {2008},
date = {2008-01-01},
urldate = {2011-10-24},
journal = {Current Biology: CB},
volume = {18},
number = {6},
pages = {435--441},
abstract = {In Drosophila, SCALLOPED (SD) belongs to a family of evolutionarily conserved proteins characterized by the presence of a TEA/ATTS DNA-binding domain [1, 2]. SD physically interacts with the product of the vestigial (vg) gene, where the dimer functions as a master gene controlling wing formation [3, 4]. The VG-SD dimer activates the transcription of several specific wing genes, including sd and vg themselves [5, 6]. The dimer drives cell-cycle progression by inducing expression of the dE2F1 transcription factor [7], which regulates genes involved in DNA replication and cell-cycle progression. Recently, YORKIE (YKI) was identified as a transcriptional coactivator that is the downstream effector of the Hippo signaling pathway, which controls cell proliferation and apoptosis in Drosophila[8]. We identified SD as a partner for YKI. We show that interaction between YKI and SD increases SD transcriptional activity both ex vivo in Drosophila S2 cells and in vivo in Drosophila wing discs and promotes YKI nuclear localization. We also show that YKI overexpression induces vg and dE2F1 expression and that proliferation induced by YKI or by a dominant-negative form of FAT in wing disc is significantly reduced in a sd hypomorphic mutant context. Contrary to YKI, SD is not required in all imaginal tissues. This indicates that YKI-SD interaction acts in a tissue-specific fashion and that other YKI partners must exist.},
keywords = {Animals, Cell Proliferation, Drosophila, Drosophila Proteins, HeLa Cells, Humans, I2CT, Imagerie, Intracellular Signaling Peptides and Proteins, Morphogenesis, Nuclear Proteins, Protein Kinases, Protein-Serine-Threonine Kinases, Signal Transduction, Trans-Activators, Transcription Factors, Tumor Suppressor Proteins, Wing},
pubstate = {published},
tppubtype = {article}
}
2005
Dostert Catherine, Jouanguy Emmanuelle, Irving Phil, Troxler Laurent, Galiana-Arnoux Delphine, Hetru Charles, Hoffmann Jules A, Imler Jean-Luc
The Jak-STAT signaling pathway is required but not sufficient for the antiviral response of drosophila Journal Article
In: Nature Immunology, vol. 6, no. 9, pp. 946–953, 2005, ISSN: 1529-2908.
Abstract | Links | BibTeX | Tags: Animals, bioinformatic, DNA-Binding Proteins, Genetic, Genetically Modified, hoffmann, imler, Insect Viruses, Janus Kinase 1, M3i, Male, Oligonucleotide Array Sequence Analysis, Promoter Regions, Protein-Tyrosine Kinases, Signal Transduction, STAT1 Transcription Factor, Trans-Activators
@article{dostert_jak-stat_2005,
title = {The Jak-STAT signaling pathway is required but not sufficient for the antiviral response of drosophila},
author = {Catherine Dostert and Emmanuelle Jouanguy and Phil Irving and Laurent Troxler and Delphine Galiana-Arnoux and Charles Hetru and Jules A Hoffmann and Jean-Luc Imler},
doi = {10.1038/ni1237},
issn = {1529-2908},
year = {2005},
date = {2005-01-01},
journal = {Nature Immunology},
volume = {6},
number = {9},
pages = {946--953},
abstract = {The response of drosophila to bacterial and fungal infections involves two signaling pathways, Toll and Imd, which both activate members of the transcription factor NF-kappaB family. Here we have studied the global transcriptional response of flies to infection with drosophila C virus. Viral infection induced a set of genes distinct from those regulated by the Toll or Imd pathways and triggered a signal transducer and activator of transcription (STAT) DNA-binding activity. Genetic experiments showed that the Jak kinase Hopscotch was involved in the control of the viral load in infected flies and was required but not sufficient for the induction of some virus-regulated genes. Our results indicate that in addition to Toll and Imd, a third, evolutionary conserved innate immunity pathway functions in drosophila and counters viral infection.},
keywords = {Animals, bioinformatic, DNA-Binding Proteins, Genetic, Genetically Modified, hoffmann, imler, Insect Viruses, Janus Kinase 1, M3i, Male, Oligonucleotide Array Sequence Analysis, Promoter Regions, Protein-Tyrosine Kinases, Signal Transduction, STAT1 Transcription Factor, Trans-Activators},
pubstate = {published},
tppubtype = {article}
}
1996
Barillas-Mury Carolina, Charlesworth A, Gross I, Richman A, Hoffmann Jules A, Kafatos Fotis C
Immune factor Gambif1, a new rel family member from the human malaria vector, Anopheles gambiae Journal Article
In: EMBO J., vol. 15, no. 17, pp. 4691–4701, 1996, ISSN: 0261-4189.
Abstract | BibTeX | Tags: Amino Acid, Animals, Anopheles, Base Sequence, Biological Transport, Cell Nucleus, Cells, Complementary, Cultured, DNA, DNA-Binding Proteins, hoffmann, Insect Proteins, Insect Vectors, M3i, NF-kappa B, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-rel, Sequence Homology, Trans-Activators, Transcriptional Activation
@article{barillas-mury_immune_1996,
title = {Immune factor Gambif1, a new rel family member from the human malaria vector, Anopheles gambiae},
author = {Carolina Barillas-Mury and A Charlesworth and I Gross and A Richman and Jules A Hoffmann and Fotis C Kafatos},
issn = {0261-4189},
year = {1996},
date = {1996-09-01},
journal = {EMBO J.},
volume = {15},
number = {17},
pages = {4691--4701},
abstract = {A novel rel family member, Gambif1 (gambiae immune factor 1), has been cloned from the human malaria vector, Anopheles gambiae, and shown to be most similar to Drosophila Dorsal and Dif. Gambif1 protein is translocated to the nucleus in fat body cells in response to bacterial challenge, although the mRNA is present at low levels at all developmental stages and is not induced by infection. DNA binding activity to the kappaB-like sites in the A.gambiae Defensin and the Drosophila Diptericin and Cecropin promoters is also induced in larval nuclear extracts following infection. Gambif1 has the ability to bind to kappaB-like sites in vitro. Co-transfection assays in Drosophila mbn-2 cells show that Gambif1 can activate transcription by interacting with the Drosophila Diptericin regulatory elements, but is not functionally equivalent to Dorsal in this assay. Gambif1 protein translocation to the nucleus and the appearance of kappaB-like DNA binding activity can serve as molecular markers of activation of the immune system and open up the possibility of studying the role of defence reactions in determining mosquito susceptibility/refractoriness to malaria infection.},
keywords = {Amino Acid, Animals, Anopheles, Base Sequence, Biological Transport, Cell Nucleus, Cells, Complementary, Cultured, DNA, DNA-Binding Proteins, hoffmann, Insect Proteins, Insect Vectors, M3i, NF-kappa B, Proto-Oncogene Proteins, Proto-Oncogene Proteins c-rel, Sequence Homology, Trans-Activators, Transcriptional Activation},
pubstate = {published},
tppubtype = {article}
}
1994
Ferrandon Dominique, Elphick L, Nüsslein-Volhard C, Johnston St D
Staufen protein associates with the 3'UTR of bicoid mRNA to form particles that move in a microtubule-dependent manner Journal Article
In: Cell, vol. 79, no. 7, pp. 1221–1232, 1994, ISSN: 0092-8674.
Abstract | BibTeX | Tags: Animals, Base Sequence, Cell Polarity, ferrandon, Homeodomain Proteins, Insect Hormones, M3i, messenger, Microtubules, Nucleic Acid Conformation, Oocytes, RNA, RNA-Binding Proteins, Trans-Activators
@article{ferrandon_staufen_1994b,
title = {Staufen protein associates with the 3'UTR of bicoid mRNA to form particles that move in a microtubule-dependent manner},
author = {Dominique Ferrandon and L Elphick and C Nüsslein-Volhard and St D Johnston},
issn = {0092-8674},
year = {1994},
date = {1994-12-01},
journal = {Cell},
volume = {79},
number = {7},
pages = {1221--1232},
abstract = {Staufen protein is required in order to anchor bicoid (bcd) mRNA at the anterior pole of the Drosophila egg. Here we show that staufen protein colocalizes with bcd mRNA at the anterior, and that this localization depends upon its association with the mRNA. Upon injection into the embryo, bcd transcripts specifically interact with staufen, and we have mapped the sequences required to three regions of the 3'UTR, each of which is predicted to form a long stem-loop. The resulting staufen-bcd 3'UTR complexes form particles that show a microtubule-dependent localization. Since staufen is also transported with oskar (osk) mRNA during oogenesis, staufen associates specifically with both osk and bcd mRNAs to mediate their localizations, but at two distinct stages of development.},
keywords = {Animals, Base Sequence, Cell Polarity, ferrandon, Homeodomain Proteins, Insect Hormones, M3i, messenger, Microtubules, Nucleic Acid Conformation, Oocytes, RNA, RNA-Binding Proteins, Trans-Activators},
pubstate = {published},
tppubtype = {article}
}