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3. A Drosophila Tumor Suppressor Gene Prevents Tonic TNF Signaling through Receptor N-Glycosylation

Author

de Vreede, Geert, Morrison, Holly A, Houser, Alexandra M, Boileau, Ryan M, Andersen, Ditte, Colombani, Julien, and Bilder, David

Subjects
Biochemistry and Cell Biology, Biological Sciences, Genetics, 1.1 Normal biological development and functioning, Underpinning research, Animals, Cell Proliferation, Drosophila Proteins, Drosophila melanogaster, Female, Genes, Tumor Suppressor, Glycosylation, Imaginal Discs, Intracellular Signaling Peptides and Proteins, JNK Mitogen-Activated Protein Kinases, Male, Mutation, Phenotype, Protein Serine-Threonine Kinases, Receptors, Tumor Necrosis Factor, Signal Transduction, Drosophila, Eiger, Grindelwald, Hippo, JNK signaling, N-linked glycosylation, TNF, TNF-α, TNFR, tumor suppressor, Medical and Health Sciences, Developmental Biology, Biochemistry and cell biology
Abstract

Drosophila tumor suppressor genes have revealed molecular pathways that control tissue growth, but mechanisms that regulate mitogenic signaling are far from understood. Here we report that the Drosophila TSG tumorous imaginal discs (tid), whose phenotypes were previously attributed to mutations in a DnaJ-like chaperone, are in fact driven by the loss of the N-linked glycosylation pathway component ALG3. tid/alg3 imaginal discs display tissue growth and architecture defects that share characteristics of both neoplastic and hyperplastic mutants. Tumorous growth is driven by inhibited Hippo signaling, induced by excess Jun N-terminal kinase (JNK) activity. We show that ectopic JNK activation is caused by aberrant glycosylation of a single protein, the fly tumor necrosis factor (TNF) receptor homolog, which results in increased binding to the continually circulating TNF. Our results suggest that N-linked glycosylation sets the threshold of TNF receptor signaling by modifying ligand-receptor interactions and that cells may alter this modification to respond appropriately to physiological cues.

Published
2018

8. The Drosophila tumor necrosis factor receptor, Wengen, couples energy expenditure with gut immunity

Author

Loudhaief, Rihab, Jneid, Rouba, Christensen, Christian Fokdal, Mackay, Duncan J, Andersen, Ditte S, and Colombani, Julien

Abstract

It is well established that tumor necrosis factor (TNF) plays an instrumental role in orchestrating the metabolic disorders associated with late stages of cancers. However, it is not clear whether TNF/TNF receptor (TNFR) signaling controls energy homeostasis in healthy individuals. Here, we show that the highly conserved Drosophila TNFR, Wengen (Wgn), is required in the enterocytes (ECs) of the adult gut to restrict lipid catabolism, suppress immune activity, and maintain tissue homeostasis. Wgn limits autophagy-dependent lipolysis by restricting cytoplasmic levels of the TNFR effector, TNFR-associated factor 3 (dTRAF3), while it suppresses immune processes through inhibition of the dTAK1/TAK1-Relish/NF-κB pathway in a dTRAF2-dependent manner. Knocking down dTRAF3 or overexpressing dTRAF2 is sufficient to suppress infection-induced lipid depletion and immune activation, respectively, showing that Wgn/TNFR functions as an intersection between metabolism and immunity allowing pathogen-induced metabolic reprogramming to fuel the energetically costly task of combatting an infection.

Published
2023
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12. TOR coordinates bulk and targeted endocytosis in the Drosophila melanogaster fat body to regulate cell growth

Author

Hennig, Krista M., Colombani, Julien, and Neufeld, Thomas P.

Subjects
Drosophila -- Physiological aspects, Cellular control mechanisms -- Research, Adenosine triphosphatase -- Research, Biological sciences
Abstract

Target of rapamycin (TOR) is a central regulator of cellular and organismal growth in response to nutrient conditions. In a genetic screen for novel TOR interactors in Drosophila melanogaster, we have identified the clathrin-uncoating ATPase Hsc70-4, which is a key regulator of endocytosis. We present genetic evidence that TOR signaling stimulates bulk endocytic uptake and inhibits the targeted endocytic degradation of the amino acid importer Slimfast. Thus, TOR simultaneously down-regulates aspects of endocytosis that inhibit growth and up-regulates potential growth-promoting functions of endocytosis. In addition, we find that disruption of endocytosis leads to changes in TOR and phosphatidylinositol-3 kinase activity, affecting cell growth, autophagy, and rapamycin sensitivity. Our data indicate that endocytosis acts both as an effector function downstream of TOR and as a physiologically relevant regulator of TOR signaling.

Published
2006

18. [Some insulins to orchestrate growth]

Author

Boone, Emilie, Boulan, Laura, Andersen, Ditte, Romero, Nuria, Léopold, Pierre, Colombani, Julien, Institut de Biologie Valrose (IBV), Université Nice Sophia Antipolis (... - 2019) (UNS), and COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA)

Subjects
MESH: Signal Transduction, MESH: Humans, MESH: Drosophila Proteins, [SDV]Life Sciences [q-bio], Insulins, Gene Expression Regulation, Developmental, MESH: Drosophila melanogaster, Drosophila melanogaster, MESH: Gene Expression Regulation, Developmental, MESH: Growth and Development, Animals, Drosophila Proteins, Humans, Intercellular Signaling Peptides and Proteins, MESH: Animals, Growth and Development, MESH: Intercellular Signaling Peptides and Proteins, MESH: Insulins, Signal Transduction
Abstract

International audience; Body size is an intrinsic property of living organisms that is intimately linked to the developmental program to produce fit individuals with proper proportions. Final size is the result of both genetic determinants and sophisticated mechanisms adapting size to available resources. Even though organs grow according to autonomous programs, some coordination mechanisms ensure that the different body parts adjust their growth with the rest of the body. In Drosophila, Dilp8, a hormone of the Insulin/Relaxin family is a key player in this inter-organs coordination and is required together with its receptor Lgr3 to limit developmental variability. Recently, the transcriptional co-activator Yki (homologue of YAP/TAZ factors in mammals) was shown to regulate dilp8 expression and contribute to the coordination of organ growth in Drosophila.

Published
2017
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22. [Targeting the appropriate body size]

Author

Colombani, Julien, Andersen, Ditte S, Leopold, Pierre, Institut de Biologie Valrose (IBV), Université Nice Sophia Antipolis (... - 2019) (UNS), and COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA)

Subjects
[SDV.BDD]Life Sciences [q-bio]/Development Biology, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2012
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23. [A nutrient sensor mechanism]

Author

Colombani, Julien, Arquier, Nathalie, Léopold, Pierre, Institut de signalisation, biologie du développement et cancer (ISBDC), Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), and COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Université Côte d'Azur (UCA)

Subjects
MESH: Signal Transduction, MESH: Drosophila, MESH: Drosophila Proteins, [SDV.BC.IC]Life Sciences [q-bio]/Cellular Biology/Cell Behavior [q-bio.CB], MESH: Animals, MESH: 1-Phosphatidylinositol 3-Kinase, MESH: Fat Body, MESH: Nutrition Physiology, ComputingMilieux_MISCELLANEOUS
Abstract

International audience

Published
2004

31. Guillain-Barré Syndrome Associated With Zika Virus Infection in Martinique in 2016: A Prospective Study

Author

Benoît, Rozé, Fatiha, Najioullah, Jean-Louis, Fergé, Frédérique, Dorléans, Kossivi, Apetse, Jose-Luis, Barnay, Elise, Daudens-Vaysse, Yannick, Brouste, Raymond, Césaire, Laurence, Fagour, Ruddy, Valentino, Martine, Ledrans, Hossein, Mehdaoui, Sylvie, Abel, Isabelle, Leparc-Goffart, Aissatou, Signate, André, Cabié, Rosalie, Vilain, Service de Maladies Infectieuses et Tropicales [Fort-de-France, Martinique], CHU Fort de France-CHU de la Martinique [Fort de France]-Hôpital Pierre Zobda-Quitman [CHU de la Martinique], CHU de la Martinique [Fort de France], Unité de soins intensifs [CHU Martinique], Hôpital Pierre Zobda-Quitman [CHU de la Martinique], CHU de la Martinique [Fort de France]-CHU de la Martinique [Fort de France], Laboratoire de Virologie-Immunologie [Fort de France, Martinique] (EA 4537), Centre Hospitalier Universitaire de Martinique [Fort-de-France, Martinique], Unité Régionale Antilles Guyane [Saint-Maurice] (Agence Nationale de la Santé Publique ), Département d'Electrophysiologie [Fort de France, Martinique], Unité de Réhabilitation [Fort de France, Martinique], Hôpital Le Lamentin Bourg [CHU de la Martinique], Service d'Urgence [Fort de France, Martinique], Institut de Recherche Biomédicale des Armées [Antenne Marseille] (IRBA), Environnement, Santé, Sociétés (ESS), Centre National de la Recherche Scientifique (CNRS), Service de neurologie [Fort-de-France, Martinique], CHU de la Martinique [Fort de France]-Hôpital Pierre Zobda-Quitman [CHU de la Martinique], CHU de la Martinique [Fort de France]-Centre Hospitalier Universitaire de Martinique [Fort-de-France, Martinique], Centre d'Investigation Clinique Antilles-Guyane (CIC - Antilles Guyane), CHU de Fort de France-Centre Hospitalier Andrée Rosemon [Cayenne, Guyane Française]-CHU Pointe-à-Pitre/Abymes [Guadeloupe] -Institut National de la Santé et de la Recherche Médicale (INSERM)-Université des Antilles et de la Guyane (UAG), This research was sponsored by University Hospital of Martinique (UHM) for regulatory and ethic submission and supported by the Clinical Research Hospital Program from the French Ministry of Health (PHRC 2009, NCT01099852). This research was support by the French network for Research and Action targeting emerging infectious diseases (REACTING)., Guillain-Barré Syndrome Zika Working Group of Martiniquea : Gwenole Jean Abgrall, Véronique Aïm, Alessandro Arrigo, Philippe Cabre, Cyrille Chabartier, Sylvie Colombani, Julien Cuziat, Christophe Deligny, Nicole Desbois, Anne-Laure Dessoy, Gaëlle Dunoyer, Régis Duvauferrier, N’Guyen Duc, Mireille Edimonana, Pierre Garrigou, Stéphane Gaucher, Sarah Gourgoudou, Karine Guitteaud, Patrick Hochedez, Gwladys Ivanes, Yolène Jacquens, Sandrine Julié, Armelle Jean-Etienne, Séverine Jeannin, Joux Julien, Pasquier Jérémie, Jean- Louis Lamaignère, Ingrid Laudarin, Maud Le Gall, Véronique Legris- Allusson, Mehdi Mejdoubi, Corinne Michel, Franck Michel, Charline Miossec, Florence Moinet, Cervantes Minerva, Claude Olive, Pascale Olive, Karine Pailla, Céline Paysant, Sandrine Pierre-François, Mathilde Pircher, Katlyne Polomat, Alain Putot, Patrick René-Corail, Dabor Resiere, Christiane Richer, Jean-Romain Risson, Karen Rome, Marie Sabia, Michel Schloesser, Pauline Simonnet-Vigeral, Rafaelle Théodose, Rosalie Vilain., Université des Antilles et de la Guyane (UAG)-Institut National de la Santé et de la Recherche Médicale (INSERM)-CHU Pointe-à-Pitre/Abymes [Guadeloupe] -CHU de Fort de France-Centre Hospitalier Andrée Rosemon [Cayenne, Guyane Française], and BUISINE, Soline

Subjects
Microbiology (medical), Male, Pediatrics, medicine.medical_specialty, 030231 tropical medicine, Guillain-Barre Syndrome, Zika virus, Serology, Disease Outbreaks, 03 medical and health sciences, 0302 clinical medicine, [SDV.MHEP.MI]Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Intensive care, Medicine, Humans, Martinique, Prospective Studies, Aged, [SDV.MP.VIR] Life Sciences [q-bio]/Microbiology and Parasitology/Virology, [SDV.MHEP.ME] Life Sciences [q-bio]/Human health and pathology/Emerging diseases, [SDV.MHEP.ME]Life Sciences [q-bio]/Human health and pathology/Emerging diseases, biology, Guillain-Barre syndrome, business.industry, Outbreak, Retrospective cohort study, vector-borne infections, Zika Virus, Middle Aged, Zika virus infection, biology.organism_classification, medicine.disease, bacterial infections and mycoses, Guillain-Barré syndrome, 3. Good health, Infectious Diseases, outbreaks, [SDV.MP.VIR]Life Sciences [q-bio]/Microbiology and Parasitology/Virology, [SDV.MHEP.MI] Life Sciences [q-bio]/Human health and pathology/Infectious diseases, Etiology, Female, business, 030217 neurology & neurosurgery
Abstract

International audience; Background: Guillain-Barré syndrome (GBS) has been reported to be associated with Zika virus (ZIKV) infection in case reports and retrospective studies, mostly on the basis of serological tests, with the problematic cross-reacting antibodies of the Flavivirus genus. Some GBS cases do not exhibit a high level of diagnostic certainty. This prospective study aimed to describe the clinical profiles and the frequency of GBS associated with ZIKV during the ZIKV outbreak in Martinique in 2016.Methods: We recorded prospective data from GBS meeting levels 1 or 2 of diagnostic certainty for the Brighton Collaboration, with proof of recent ZIKV infection and negative screening for etiologies of GBS.Results: Of the sample of 34 patients with suspected GBS during the outbreak, 30 had a proven presence of GBS, and 23 had a recent ZIKV infection. The estimated GBS incidence rate ratio (2016 vs 2006-2015) was 4.52 (95% confidence interval, 2.80-7.64; P = .0001). Recent ZIKV infection was confirmed by urine reverse-transcription polymerase chain reaction (RT-PCR) analysis in 17 cases and by serology in 6 cases. Patients, 65% of whom were male, had a median age of 61 years (interquartile range, 56-71 years) and experienced severe GBS. Electrophysiological tests were consistent with the primary demyelinating form of the disease.Conclusions: ZIKV infection is usually benign, when symptomatic, but in countries at risk of ZIKV epidemics, adequate intensive care bed capacity is required for management of severe GBS cases. Arbovirus RNA detection by RT-PCR should be part of the management of GBS cases.

Published
2017
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32. The Drosophila TNF receptor Grindelwald couples loss of cell polarity and neoplastic growth

Author

Ditte S. Andersen, Valentina Palmerini, Krittalak Chakrabandhu, Julien Colombani, Janine Toggweiler, Michael Röthlisberger, Konrad Basler, Emilie Boone, Marina Mapelli, Pierre Léopold, Anne-Odile Hueber, Institut de Biologie Valrose (IBV), Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), University of Zurich, and Colombani, Julien

Subjects
Male, [SDV]Life Sciences [q-bio], Apoptosis, MESH: Amino Acid Sequence, Receptors, Tumor Necrosis Factor, 0302 clinical medicine, Neoplasms, Cell polarity, Drosophila Proteins, MESH: Animals, MESH: Neoplasms, Receptor, [SDV.BDD]Life Sciences [q-bio]/Development Biology, ComputingMilieux_MISCELLANEOUS, Epithelial polarity, 0303 health sciences, Multidisciplinary, Cell Polarity, Anatomy, 10124 Institute of Molecular Life Sciences, Transmembrane protein, Cell biology, Cell Transformation, Neoplastic, Drosophila melanogaster, 030220 oncology & carcinogenesis, MESH: Cell Adhesion Molecules, MESH: Cell Division, Female, MESH: Membrane Proteins, MESH: Cell Polarity, Matrix Metalloproteinase 1, MESH: ras Proteins, Cell Division, SCRIB, Programmed cell death, Polarity (physics), MESH: Drosophila Proteins, MAP Kinase Signaling System, Molecular Sequence Data, Biology, MESH: Drosophila melanogaster, 03 medical and health sciences, Animals, Humans, Neoplasm Invasiveness, Amino Acid Sequence, 030304 developmental biology, 1000 Multidisciplinary, MESH: Humans, MESH: Molecular Sequence Data, MESH: MAP Kinase Signaling System, MESH: Apoptosis, JNK Mitogen-Activated Protein Kinases, Membrane Proteins, MESH: JNK Mitogen-Activated Protein Kinases, MESH: Neoplasm Invasiveness, MESH: Receptors, Tumor Necrosis Factor, MESH: Male, MESH: Matrix Metalloproteinase 1, Disease Models, Animal, MESH: Cell Transformation, Neoplastic, ras Proteins, 570 Life sciences, biology, MESH: Disease Models, Animal, MESH: Female, Cell Adhesion Molecules, Genetic screen
Abstract

International audience; Disruption of epithelial polarity is a key event in the acquisition of neoplastic growth. JNK signalling is known to play an important part in driving the malignant progression of many epithelial tumours, although the link between loss of polarity and JNK signalling remains elusive. In a Drosophila genome-wide genetic screen designed to identify molecules implicated in neoplastic growth, we identified grindelwald (grnd), a gene encoding a transmembrane protein with homology to members of the tumour necrosis factor receptor (TNFR) superfamily. Here we show that Grnd mediates the pro-apoptotic functions of Eiger (Egr), the unique Drosophila TNF, and that overexpression of an active form of Grnd lacking the extracellular domain is sufficient to activate JNK signalling in vivo. Grnd also promotes the invasiveness of Ras(V12)/scrib(-/-) tumours through Egr-dependent Matrix metalloprotease-1 (Mmp1) expression. Grnd localizes to the subapical membrane domain with the cell polarity determinant Crumbs (Crb) and couples Crb-induced loss of polarity with JNK activation and neoplastic growth through physical interaction with Veli (also known as Lin-7). Therefore, Grnd represents the first example of a TNFR that integrates signals from both Egr and apical polarity determinants to induce JNK-dependent cell death or tumour growth.

Published
2013
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33. [Some insulins to orchestrate growth].

Author

Boone E, Boulan L, Andersen DS, Romero N, Léopold P, and Colombani J

Subjects
Animals, Drosophila Proteins genetics, Drosophila Proteins pharmacology, Drosophila Proteins physiology, Drosophila melanogaster genetics, Drosophila melanogaster growth & development, Gene Expression Regulation, Developmental drug effects, Humans, Insulins genetics, Insulins pharmacology, Intercellular Signaling Peptides and Proteins genetics, Intercellular Signaling Peptides and Proteins pharmacology, Intercellular Signaling Peptides and Proteins physiology, Signal Transduction drug effects, Growth and Development drug effects, Growth and Development genetics, Insulins physiology
Abstract

Body size is an intrinsic property of living organisms that is intimately linked to the developmental program to produce fit individuals with proper proportions. Final size is the result of both genetic determinants and sophisticated mechanisms adapting size to available resources. Even though organs grow according to autonomous programs, some coordination mechanisms ensure that the different body parts adjust their growth with the rest of the body. In Drosophila, Dilp8, a hormone of the Insulin/Relaxin family is a key player in this inter-organs coordination and is required together with its receptor Lgr3 to limit developmental variability. Recently, the transcriptional co-activator Yki (homologue of YAP/TAZ factors in mammals) was shown to regulate dilp8 expression and contribute to the coordination of organ growth in Drosophila., (© 2017 médecine/sciences – Inserm.)

Published
2017
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34. [Targeting the appropriate body size].

Author

Colombani J, Andersen DS, and Leopold P

Subjects
Animals, Drosophila melanogaster genetics, Drosophila melanogaster ultrastructure, Larva, Mammals growth & development, Metamorphosis, Biological physiology, Models, Biological, Organ Size, Organogenesis physiology, Regeneration physiology, Body Size, Drosophila Proteins physiology, Drosophila melanogaster growth & development, Intercellular Signaling Peptides and Proteins physiology
Published
2012
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36. [A nutrient sensor mechanism].

Author

Colombani J, Arquier N, and Léopold P

Subjects
Animals, Drosophila Proteins metabolism, Fat Body metabolism, Phosphatidylinositol 3-Kinases metabolism, Protein Kinases, Signal Transduction physiology, TOR Serine-Threonine Kinases, Drosophila growth & development, Nutritional Physiological Phenomena physiology
Published
2004
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