79 research outputs found

    Control of non-autonomous cell survival and overgrowth and autonomous apoptosis by members of the ESCRT-II complex

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    Die Aufrechterhaltung der IntegritĂ€t fĂŒr die SignalĂŒbertragung zwischen Zellen ist eine notwendige Voraussetzung fĂŒr die Homöostase im Organismus. Die Sortierung von Proteinen als Rezeptoren am frĂŒhen Endosom spielt dabei eine wichtige Rolle sowohl fĂŒr die Übertragung des Signals als auch die Inaktivierung des Rezeptors. Regulatorische VerĂ€nderungen in diesem Prozess können unter anderem zur Entstehung von Krankheiten wie unter anderem auch der Krebsentwicklung beitragen. In einem genetischen Screen fĂŒr Suppressoren des proapoptotischen Gens hid in Drosophila haben wir zwei Allele von vps25 identifiziert. Vps25 ist eine Komponente der ESCRT Maschinerie, die fĂŒr die Sortierung von Proteinen am frĂŒhen Endosom benötigt wird. Paradoxerweise wurden vps25 Mosaike als Suppressoren von hid-induzierter Apoptose identifiziert obwohl Zellen, die mutant fĂŒr vps25 sind, sterben. Wir zeigen jedoch, daß die nichtautonome Erhöhung von Diap1 Protein, einem Apoptoseinhibitor, fĂŒr die Suppression von hid verantwortlich ist. DarĂŒberhinaus lösen Klone die mutant fuer vps25 sind nichtautonome Proliferation durch eine Störung im Abbau des Notch Rezeptors aus, dessen ektopische Aktivierung zur Stimulation des mitogenen JAK/STAT Signalweges fĂŒhrt. Der apoptotische PhĂ€notyp von mutantem vps25 Gewebe ist das Resultat autonomer Aktivierung von mindestens zwei Zelltod Signalwegen. Sowohl Hid als auch JNK tragen zur Apoptose von vps25 mutanten Zellen bei. Eine Inhibition von Zelltod in vps25 Klonen verursacht starke ÜberwachstumsphĂ€notypen. Desweiteren ist die SignalĂŒbertragung durch den Hippo Signalweg in vps25 Klonen erhöht und hippo Mutanten blockieren Apoptose vollstĂ€ndig in vps25 Klonen. Wir fĂŒhren auch eine Analyse der anderen ESCRT-II Komponenten vps22 und vps36 durch. Wie im Fall von vps25 zeichnen sich vps22 und vps36 Mutanten durch endosomale Defekte aus, die in erhöhter Notch und JAK/STAT SignalĂŒbertragung und automomem Zelltod resultieren. Überraschenderweise haben vps22 Mutanten keine Auswirkung auf nichtautonome apoptotische Resistenz, verursachen aber starkes nichtautonomes Überwachstum. vps36 Mutanten weisen hingegen einen reziproken PhĂ€notyp auf, der sich durch eine Erhöhung der apoptotischen Resistenz auszeichnet, aber kaum nichtautonome Proliferation beeinflusst. Obwohl also vps22, vps25 und vps36 eine innige physikalische Verwandtschaft als ESCRT-II Komponenten teilen, haben sie verschiedenartige genetische Eigenschaften. Zusammenfassend lĂ€sst sich sagen, dass die phĂ€notypische Analyse von vps22, vps25 und vps36 Mutanten die Notwendigkeit der Regulation von Rezeptoren durch Sortierung von Proteinen am frĂŒhen Endosom hervorhebt, um eine adaequate Gewebshomöostase zu gewĂ€hrleisten und ein Modell zu einem besseren VerstĂ€ndnis der Mechanismen bereitstellt, die zur Krebsentstehung im Menschen beitragen

    The histone deacetylase complex MiDAC regulates a neurodevelopmental gene expression program to control neurite outgrowth

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    The mitotic deacetylase complex (MiDAC) is a recently identified histone deacetylase (HDAC) complex. While other HDAC complexes have been implicated in neurogenesis, the physiological role of MiDAC remains unknown. Here, we show that MiDAC constitutes an important regulator of neural differentiation. We demonstrate that MiDAC functions as a modulator of a neurodevelopmental gene expression program and binds to important regulators of neurite outgrowth. MiDAC upregulates gene expression of pro-neural genes such as those encoding the secreted ligands SLIT3 and NETRIN1 (NTN1) by a mechanism suggestive of H4K20ac removal on promoters and enhancers. Conversely, MiDAC inhibits gene expression by reducing H3K27ac on promoter-proximal and -distal elements of negative regulators of neurogenesis. Furthermore, loss of MiDAC results in neurite outgrowth defects that can be rescued by supplementation with SLIT3 and/or NTN1. These findings indicate a crucial role for MiDAC in regulating the ligands of the SLIT3 and NTN1 signaling axes to ensure the proper integrity of neurite development

    Common and Distinct Genetic Properties of ESCRT-II Components in Drosophila

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    BACKGROUND: Genetic studies in yeast have identified class E vps genes that form the ESCRT complexes required for protein sorting at the early endosome. In Drosophila, mutations of the ESCRT-II component vps25 cause endosomal defects leading to accumulation of Notch protein and increased Notch pathway activity. These endosomal and signaling defects are thought to account for several phenotypes. Depending on the developmental context, two different types of overgrowth can be detected. Tissue predominantly mutant for vps25 displays neoplastic tumor characteristics. In contrast, vps25 mutant clones in a wild-type background trigger hyperplastic overgrowth in a non-autonomous manner. In addition, vps25 mutant clones also promote apoptotic resistance in a non-autonomous manner. PRINCIPAL FINDINGS: Here, we genetically characterize the remaining ESCRT-II components vps22 and vps36. Like vps25, mutants of vps22 and vps36 display endosomal defects, accumulate Notch protein and--when the tissue is predominantly mutant--show neoplastic tumor characteristics. However, despite these common phenotypes, they have distinct non-autonomous phenotypes. While vps22 mutations cause strong non-autonomous overgrowth, they do not affect apoptotic resistance. In contrast, vps36 mutations increase apoptotic resistance, but have little effect on non-autonomous proliferation. Further characterization reveals that although all ESCRT-II mutants accumulate Notch protein, only vps22 and vps25 mutations trigger Notch activity. CONCLUSIONS/SIGNIFICANCE: The ESCRT-II components vps22, vps25 and vps36 display common and distinct genetic properties. Our data redefine the role of Notch for hyperplastic and neoplastic overgrowth in these mutants. While Notch is required for hyperplastic growth, it appears to be dispensable for neoplastic transformation

    TRY plant trait database – enhanced coverage and open access

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    Plant traits - the morphological, anatomical, physiological, biochemical and phenological characteristics of plants - determine how plants respond to environmental factors, affect other trophic levels, and influence ecosystem properties and their benefits and detriments to people. Plant trait data thus represent the basis for a vast area of research spanning from evolutionary biology, community and functional ecology, to biodiversity conservation, ecosystem and landscape management, restoration, biogeography and earth system modelling. Since its foundation in 2007, the TRY database of plant traits has grown continuously. It now provides unprecedented data coverage under an open access data policy and is the main plant trait database used by the research community worldwide. Increasingly, the TRY database also supports new frontiers of trait‐based plant research, including the identification of data gaps and the subsequent mobilization or measurement of new data. To support this development, in this article we evaluate the extent of the trait data compiled in TRY and analyse emerging patterns of data coverage and representativeness. Best species coverage is achieved for categorical traits - almost complete coverage for ‘plant growth form’. However, most traits relevant for ecology and vegetation modelling are characterized by continuous intraspecific variation and trait–environmental relationships. These traits have to be measured on individual plants in their respective environment. Despite unprecedented data coverage, we observe a humbling lack of completeness and representativeness of these continuous traits in many aspects. We, therefore, conclude that reducing data gaps and biases in the TRY database remains a key challenge and requires a coordinated approach to data mobilization and trait measurements. This can only be achieved in collaboration with other initiatives

    The harlequin ladybird, Harmonia axyridis: global perspectives on invasion history and ecology

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    The harlequin ladybird, Harmonia axyridis (Pallas) (Coleoptera: Coccinellidae), is native to Asia but has been intentionally introduced to many countries as a biological control agent of pest insects. In numerous countries, however, it has been introduced unintentionally. The dramatic spread of H. axyridis within many countries has been met with considerable trepidation. It is a generalist top predator, able to thrive in many habitats and across wide climatic conditions. It poses a threat to biodiversity, particularly aphidophagous insects, through competition and predation, and in many countries adverse effects have been reported on other species, particularly coccinellids. However, the patterns are not consistent around the world and seem to be affected by many factors including landscape and climate. Research on H. axyridis has provided detailed insights into invasion biology from broad patterns and processes to approaches in surveillance and monitoring. An impressive number of studies on this alien species have provided mechanistic evidence alongside models explaining large-scale patterns and processes. The involvement of citizens in monitoring this species in a number of countries around the world is inspiring and has provided data on scales that would be otherwise unachievable. Harmonia axyridis has successfully been used as a model invasive alien species and has been the inspiration for global collaborations at various scales. There is considerable scope to expand the research and associated collaborations, particularly to increase the breadth of parallel studies conducted in the native and invaded regions. Indeed a qualitative comparison of biological traits across the native and invaded range suggests that there are differences which ultimately could influence the population dynamics of this invader. Here we provide an overview of the invasion history and ecology of H. axyridis globally with consideration of future research perspectives. We reflect broadly on the contributions of such research to our understanding of invasion biology while also informing policy and people

    AnĂĄlise de PolĂ­tica Externa e PolĂ­tica Externa Brasileira: trajetĂłria, desafios e possibilidades de um campo de estudos

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    TRY plant trait database – enhanced coverage and open access

    Get PDF
    Plant traits—the morphological, anatomical, physiological, biochemical and phenological characteristics of plants—determine how plants respond to environmental factors, affect other trophic levels, and influence ecosystem properties and their benefits and detriments to people. Plant trait data thus represent the basis for a vast area of research spanning from evolutionary biology, community and functional ecology, to biodiversity conservation, ecosystem and landscape management, restoration, biogeography and earth system modelling. Since its foundation in 2007, the TRY database of plant traits has grown continuously. It now provides unprecedented data coverage under an open access data policy and is the main plant trait database used by the research community worldwide. Increasingly, the TRY database also supports new frontiers of trait-based plant research, including the identification of data gaps and the subsequent mobilization or measurement of new data. To support this development, in this article we evaluate the extent of the trait data compiled in TRY and analyse emerging patterns of data coverage and representativeness. Best species coverage is achieved for categorical traits—almost complete coverage for ‘plant growth form’. However, most traits relevant for ecology and vegetation modelling are characterized by continuous intraspecific variation and trait–environmental relationships. These traits have to be measured on individual plants in their respective environment. Despite unprecedented data coverage, we observe a humbling lack of completeness and representativeness of these continuous traits in many aspects. We, therefore, conclude that reducing data gaps and biases in the TRY database remains a key challenge and requires a coordinated approach to data mobilization and trait measurements. This can only be achieved in collaboration with other initiatives.Rest of authors: Decky Junaedi, Robert R. Junker, Eric Justes, Richard Kabzems, Jeffrey Kane, Zdenek Kaplan, Teja Kattenborn, Lyudmila Kavelenova, Elizabeth Kearsley, Anne Kempel, Tanaka Kenzo, Andrew Kerkhoff, Mohammed I. Khalil, Nicole L. Kinlock, Wilm Daniel Kissling, Kaoru Kitajima, Thomas Kitzberger, Rasmus KjĂžller, Tamir Klein, Michael Kleyer, Jitka KlimeĆĄovĂĄ, Joice Klipel, Brian Kloeppel, Stefan Klotz, Johannes M. H. Knops, Takashi Kohyama, Fumito Koike, Johannes Kollmann, Benjamin Komac, Kimberly Komatsu, Christian König, Nathan J. B. Kraft, Koen Kramer, Holger Kreft, Ingolf KĂŒhn, Dushan Kumarathunge, Jonas Kuppler, Hiroko Kurokawa, Yoko Kurosawa, Shem Kuyah, Jean-Paul Laclau, Benoit Lafleur, Erik Lallai, Eric Lamb, Andrea Lamprecht, Daniel J. Larkin, Daniel Laughlin, Yoann Le Bagousse-Pinguet, Guerric le Maire, Peter C. le Roux, Elizabeth le Roux, Tali Lee, Frederic Lens, Simon L. Lewis, Barbara Lhotsky, Yuanzhi Li, Xine Li, Jeremy W. Lichstein, Mario Liebergesell, Jun Ying Lim, Yan-Shih Lin, Juan Carlos Linares, Chunjiang Liu, Daijun Liu, Udayangani Liu, Stuart Livingstone, Joan LlusiĂ , Madelon Lohbeck, Álvaro LĂłpez-GarcĂ­a, Gabriela Lopez-Gonzalez, Zdeƈka LososovĂĄ, FrĂ©dĂ©rique Louault, BalĂĄzs A. LukĂĄcs, Petr LukeĆĄ, Yunjian Luo, Michele Lussu, Siyan Ma, Camilla Maciel Rabelo Pereira, Michelle Mack, Vincent Maire, Annikki MĂ€kelĂ€, Harri MĂ€kinen, Ana Claudia Mendes Malhado, Azim Mallik, Peter Manning, Stefano Manzoni, Zuleica Marchetti, Luca Marchino, Vinicius Marcilio-Silva, Eric Marcon, Michela Marignani, Lars Markesteijn, Adam Martin, Cristina MartĂ­nez-Garza, Jordi MartĂ­nez-Vilalta, Tereza MaĆĄkovĂĄ, Kelly Mason, Norman Mason, Tara Joy Massad, Jacynthe Masse, Itay Mayrose, James McCarthy, M. Luke McCormack, Katherine McCulloh, Ian R. McFadden, Brian J. McGill, Mara Y. McPartland, Juliana S. Medeiros, Belinda Medlyn, Pierre Meerts, Zia Mehrabi, Patrick Meir, Felipe P. L. Melo, Maurizio Mencuccini, CĂ©line Meredieu, Julie Messier, Ilona MĂ©szĂĄros, Juha Metsaranta, Sean T. Michaletz, Chrysanthi Michelaki, Svetlana Migalina, Ruben Milla, Jesse E. D. Miller, Vanessa Minden, Ray Ming, Karel Mokany, Angela T. Moles, Attila MolnĂĄr V, Jane Molofsky, Martin Molz, Rebecca A. Montgomery, Arnaud Monty, Lenka MoravcovĂĄ, Alvaro Moreno-MartĂ­nez, Marco Moretti, Akira S. Mori, Shigeta Mori, Dave Morris, Jane Morrison, Ladislav Mucina, Sandra Mueller, Christopher D. Muir, Sandra Cristina MĂŒller, François Munoz, Isla H. Myers-Smith, Randall W. Myster, Masahiro Nagano, Shawna Naidu, Ayyappan Narayanan, Balachandran Natesan, Luka Negoita, Andrew S. Nelson, Eike Lena Neuschulz, Jian Ni, Georg Niedrist, Jhon Nieto, Ülo Niinemets, Rachael Nolan, Henning Nottebrock, Yann Nouvellon, Alexander Novakovskiy, The Nutrient Network, Kristin Odden Nystuen, Anthony O'Grady, Kevin O'Hara, Andrew O'Reilly-Nugent, Simon Oakley, Walter Oberhuber, Toshiyuki Ohtsuka, Ricardo Oliveira, Kinga Öllerer, Mark E. Olson, Vladimir Onipchenko, Yusuke Onoda, Renske E. Onstein, Jenny C. Ordonez, Noriyuki Osada, Ivika Ostonen, Gianluigi Ottaviani, Sarah Otto, Gerhard E. Overbeck, Wim A. Ozinga, Anna T. Pahl, C. E. Timothy Paine, Robin J. Pakeman, Aristotelis C. Papageorgiou, Evgeniya Parfionova, Meelis PĂ€rtel, Marco Patacca, Susana Paula, Juraj Paule, Harald Pauli, Juli G. Pausas, Begoña Peco, Josep Penuelas, Antonio Perea, Pablo Luis Peri, Ana Carolina Petisco-Souza, Alessandro Petraglia, Any Mary Petritan, Oliver L. Phillips, Simon Pierce, ValĂ©rio D. Pillar, Jan Pisek, Alexandr Pomogaybin, Hendrik Poorter, Angelika Portsmuth, Peter Poschlod, Catherine Potvin, Devon Pounds, A. Shafer Powell, Sally A. Power, Andreas Prinzing, Giacomo Puglielli, Petr PyĆĄek, Valerie Raevel, Anja Rammig, Johannes Ransijn, Courtenay A. Ray, Peter B. Reich, Markus Reichstein, Douglas E. B. Reid, Maxime RĂ©jou-MĂ©chain, Victor Resco de Dios, Sabina Ribeiro, Sarah Richardson, Kersti Riibak, Matthias C. Rillig, Fiamma Riviera, Elisabeth M. R. Robert, Scott Roberts, Bjorn Robroek, Adam Roddy, Arthur Vinicius Rodrigues, Alistair Rogers, Emily Rollinson, Victor Rolo, Christine Römermann, Dina Ronzhina, Christiane Roscher, Julieta A. Rosell, Milena Fermina Rosenfield, Christian Rossi, David B. Roy, Samuel Royer-Tardif, Nadja RĂŒger, Ricardo Ruiz-Peinado, Sabine B. Rumpf, Graciela M. Rusch, Masahiro Ryo, Lawren Sack, Angela Saldaña, Beatriz Salgado-Negret, Roberto Salguero-Gomez, Ignacio Santa-Regina, Ana Carolina Santacruz-GarcĂ­a, Joaquim Santos, Jordi Sardans, Brandon Schamp, Michael Scherer-Lorenzen, Matthias Schleuning, Bernhard Schmid, Marco Schmidt, Sylvain Schmitt, Julio V. Schneider, Simon D. Schowanek, Julian Schrader, Franziska Schrodt, Bernhard Schuldt, Frank Schurr, Galia Selaya Garvizu, Marina Semchenko, Colleen Seymour, Julia C. Sfair, Joanne M. Sharpe, Christine S. Sheppard, Serge Sheremetiev, Satomi Shiodera, Bill Shipley, Tanvir Ahmed Shovon, Alrun SiebenkĂ€s, Carlos Sierra, Vasco Silva, Mateus Silva, Tommaso Sitzia, Henrik Sjöman, Martijn Slot, Nicholas G. Smith, Darwin Sodhi, Pamela Soltis, Douglas Soltis, Ben Somers, GrĂ©gory Sonnier, Mia Vedel SĂžrensen, Enio Egon Sosinski Jr, Nadejda A. Soudzilovskaia, Alexandre F. Souza, Marko Spasojevic, Marta Gaia Sperandii, Amanda B. Stan, James Stegen, Klaus Steinbauer, Jörg G. Stephan, Frank Sterck, Dejan B. Stojanovic, Tanya Strydom, Maria Laura Suarez, Jens-Christian Svenning, Ivana SvitkovĂĄ, Marek Svitok, Miroslav Svoboda, Emily Swaine, Nathan Swenson, Marcelo Tabarelli, Kentaro Takagi, Ulrike Tappeiner, RubĂ©n Tarifa, Simon Tauugourdeau, Cagatay Tavsanoglu, Mariska te Beest, Leho Tedersoo, Nelson Thiffault, Dominik Thom, Evert Thomas, Ken Thompson, Peter E. Thornton, Wilfried Thuiller, LubomĂ­r TichĂœ, David Tissue, Mark G. Tjoelker, David Yue Phin Tng, Joseph Tobias, PĂ©ter Török, Tonantzin Tarin, JosĂ© M. Torres-Ruiz, BĂ©la TĂłthmĂ©rĂ©sz, Martina Treurnicht, Valeria Trivellone, Franck Trolliet, Volodymyr Trotsiuk, James L. Tsakalos, Ioannis Tsiripidis, Niklas Tysklind, Toru Umehara, Vladimir Usoltsev, Matthew Vadeboncoeur, Jamil Vaezi, Fernando Valladares, Jana Vamosi, Peter M. van Bodegom, Michiel van Breugel, Elisa Van Cleemput, Martine van de Weg, Stephni van der Merwe, Fons van der Plas, Masha T. van der Sande, Mark van Kleunen, Koenraad Van Meerbeek, Mark Vanderwel, Kim AndrĂ© Vanselow, Angelica VĂ„rhammar, Laura Varone, Maribel Yesenia Vasquez Valderrama, Kiril Vassilev, Mark Vellend, Erik J. Veneklaas, Hans Verbeeck, Kris Verheyen, Alexander Vibrans, Ima Vieira, Jaime VillacĂ­s, Cyrille Violle, Pandi Vivek, Katrin Wagner, Matthew Waldram, Anthony Waldron, Anthony P. Walker, Martyn Waller, Gabriel Walther, Han Wang, Feng Wang, Weiqi Wang, Harry Watkins, James Watkins, Ulrich Weber, James T. Weedon, Liping Wei, Patrick Weigelt, Evan Weiher, Aidan W. Wells, Camilla Wellstein, Elizabeth Wenk, Mark Westoby, Alana Westwood, Philip John White, Mark Whitten, Mathew Williams, Daniel E. Winkler, Klaus Winter, Chevonne Womack, Ian J. Wright, S. Joseph Wright, Justin Wright, Bruno X. Pinho, Fabiano Ximenes, Toshihiro Yamada, Keiko Yamaji, Ruth Yanai, Nikolay Yankov, Benjamin Yguel, KĂĄtia Janaina Zanini, Amy E. Zanne, David ZelenĂœ, Yun-Peng Zhao, Jingming Zheng, Ji Zheng, Kasia ZiemiƄska, Chad R. Zirbel, Georg Zizka, IriĂ© Casimir Zo-Bi, Gerhard Zotz, Christian Wirth.Max Planck Institute for Biogeochemistry; Max Planck Society; German Centre for Integrative Biodiversity Research (iDiv) Halle-Jena-Leipzig; International Programme of Biodiversity Science (DIVERSITAS); International Geosphere-Biosphere Programme (IGBP); Future Earth; French Foundation for Biodiversity Research (FRB); GIS ‘Climat, Environnement et SociĂ©tĂ©'.http://wileyonlinelibrary.com/journal/gcbhj2021Plant Production and Soil Scienc
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