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  • 1
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    Unique role for ATG5 in neutrophil-mediated immunopathology during M. tuberculosis infection (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-12-10
    Description: Mycobacterium tuberculosis, a major global health threat, replicates in macrophages in part by inhibiting phagosome-lysosome fusion, until interferon-gamma (IFNgamma) activates the macrophage to traffic M. tuberculosis to the lysosome. How IFNgamma elicits this effect is unknown, but many studies suggest a role for macroautophagy (herein termed autophagy), a process by which cytoplasmic contents are targeted for lysosomal degradation. The involvement of autophagy has been defined based on studies in cultured cells where M. tuberculosis co-localizes with autophagy factors ATG5, ATG12, ATG16L1, p62, NDP52, BECN1 and LC3 (refs 2-6), stimulation of autophagy increases bacterial killing, and inhibition of autophagy increases bacterial survival. Notably, these studies reveal modest (~1.5-3-fold change) effects on M. tuberculosis replication. By contrast, mice lacking ATG5 in monocyte-derived cells and neutrophils (polymorponuclear cells, PMNs) succumb to M. tuberculosis within 30 days, an extremely severe phenotype similar to mice lacking IFNgamma signalling. Importantly, ATG5 is the only autophagy factor that has been studied during M. tuberculosis infection in vivo and autophagy-independent functions of ATG5 have been described. For this reason, we used a genetic approach to elucidate the role for multiple autophagy-related genes and the requirement for autophagy in resistance to M. tuberculosis infection in vivo. Here we show that, contrary to expectation, autophagic capacity does not correlate with the outcome of M. tuberculosis infection. Instead, ATG5 plays a unique role in protection against M. tuberculosis by preventing PMN-mediated immunopathology. Furthermore, while Atg5 is dispensable in alveolar macrophages during M. tuberculosis infection, loss of Atg5 in PMNs can sensitize mice to M. tuberculosis. These findings shift our understanding of the role of ATG5 during M. tuberculosis infection, reveal new outcomes of ATG5 activity, and shed light on early events in innate immunity that are required to regulate disease pathology and bacterial replication.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kimmey, Jacqueline M -- Huynh, Jeremy P -- Weiss, Leslie A -- Park, Sunmin -- Kambal, Amal -- Debnath, Jayanta -- Virgin, Herbert W -- Stallings, Christina L -- GM007067/GM/NIGMS NIH HHS/ -- U19 AI109725/AI/NIAID NIH HHS/ -- England -- Nature. 2015 Dec 24;528(7583):565-9. doi: 10.1038/nature16451. Epub 2015 Dec 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Microbiology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St Louis, Missouri 63110, USA. ; Department of Pathology and Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, California 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26649827" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autophagy/genetics ; Dendritic Cells/immunology/metabolism ; Female ; Immunity, Innate/immunology ; Interferon-gamma/deficiency/immunology ; Macrophages, Alveolar/immunology/metabolism ; Male ; Mice ; Microtubule-Associated Proteins/deficiency/*metabolism ; *Mycobacterium tuberculosis/immunology/physiology ; Neutrophils/*immunology/metabolism ; Tuberculosis/*immunology/microbiology/*pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Lineage correlations of single cell division time as a probe of cell-cycle dynamics (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-03-13
    Description: Stochastic processes in cells are associated with fluctuations in mRNA, protein production and degradation, noisy partition of cellular components at division, and other cell processes. Variability within a clonal population of cells originates from such stochastic processes, which may be amplified or reduced by deterministic factors. Cell-to-cell variability, such as that seen in the heterogeneous response of bacteria to antibiotics, or of cancer cells to treatment, is understood as the inevitable consequence of stochasticity. Variability in cell-cycle duration was observed long ago; however, its sources are still unknown. A central question is whether the variance of the observed distribution originates from stochastic processes, or whether it arises mostly from a deterministic process that only appears to be random. A surprising feature of cell-cycle-duration inheritance is that it seems to be lost within one generation but to be still present in the next generation, generating poor correlation between mother and daughter cells but high correlation between cousin cells. This observation suggests the existence of underlying deterministic factors that determine the main part of cell-to-cell variability. We developed an experimental system that precisely measures the cell-cycle duration of thousands of mammalian cells along several generations and a mathematical framework that allows discrimination between stochastic and deterministic processes in lineages of cells. We show that the inter- and intra-generation correlations reveal complex inheritance of the cell-cycle duration. Finally, we build a deterministic nonlinear toy model for cell-cycle inheritance that reproduces the main features of our data. Our approach constitutes a general method to identify deterministic variability in lineages of cells or organisms, which may help to predict and, eventually, reduce cell-to-cell heterogeneity in various systems, such as cancer cells under treatment.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sandler, Oded -- Mizrahi, Sivan Pearl -- Weiss, Noga -- Agam, Oded -- Simon, Itamar -- Balaban, Nathalie Q -- England -- Nature. 2015 Mar 26;519(7544):468-71. doi: 10.1038/nature14318. Epub 2015 Mar 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Molecular Genetics, IMRIC, The Hebrew University Hadassah Medical School, Jerusalem 91120, Israel. ; 1] Department of Microbiology and Molecular Genetics, IMRIC, The Hebrew University Hadassah Medical School, Jerusalem 91120, Israel [2] Racah Institute of Physics, Edmond J. Safra Campus, The Hebrew University, Jerusalem 91904, Israel. ; Racah Institute of Physics, Edmond J. Safra Campus, The Hebrew University, Jerusalem 91904, Israel.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25762143" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology ; Cell Cycle/drug effects/*genetics ; Cell Division/drug effects/genetics ; Cell Line ; *Cell Lineage ; Mammals ; Models, Biological ; Stochastic Processes ; Time Factors
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 3
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    Tumour exosome integrins determine organotropic metastasis (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-11-03
    Description: Ever since Stephen Paget's 1889 hypothesis, metastatic organotropism has remained one of cancer's greatest mysteries. Here we demonstrate that exosomes from mouse and human lung-, liver- and brain-tropic tumour cells fuse preferentially with resident cells at their predicted destination, namely lung fibroblasts and epithelial cells, liver Kupffer cells and brain endothelial cells. We show that tumour-derived exosomes uptaken by organ-specific cells prepare the pre-metastatic niche. Treatment with exosomes from lung-tropic models redirected the metastasis of bone-tropic tumour cells. Exosome proteomics revealed distinct integrin expression patterns, in which the exosomal integrins alpha6beta4 and alpha6beta1 were associated with lung metastasis, while exosomal integrin alphavbeta5 was linked to liver metastasis. Targeting the integrins alpha6beta4 and alphavbeta5 decreased exosome uptake, as well as lung and liver metastasis, respectively. We demonstrate that exosome integrin uptake by resident cells activates Src phosphorylation and pro-inflammatory S100 gene expression. Finally, our clinical data indicate that exosomal integrins could be used to predict organ-specific metastasis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hoshino, Ayuko -- Costa-Silva, Bruno -- Shen, Tang-Long -- Rodrigues, Goncalo -- Hashimoto, Ayako -- Tesic Mark, Milica -- Molina, Henrik -- Kohsaka, Shinji -- Di Giannatale, Angela -- Ceder, Sophia -- Singh, Swarnima -- Williams, Caitlin -- Soplop, Nadine -- Uryu, Kunihiro -- Pharmer, Lindsay -- King, Tari -- Bojmar, Linda -- Davies, Alexander E -- Ararso, Yonathan -- Zhang, Tuo -- Zhang, Haiying -- Hernandez, Jonathan -- Weiss, Joshua M -- Dumont-Cole, Vanessa D -- Kramer, Kimberly -- Wexler, Leonard H -- Narendran, Aru -- Schwartz, Gary K -- Healey, John H -- Sandstrom, Per -- Labori, Knut Jorgen -- Kure, Elin H -- Grandgenett, Paul M -- Hollingsworth, Michael A -- de Sousa, Maria -- Kaur, Sukhwinder -- Jain, Maneesh -- Mallya, Kavita -- Batra, Surinder K -- Jarnagin, William R -- Brady, Mary S -- Fodstad, Oystein -- Muller, Volkmar -- Pantel, Klaus -- Minn, Andy J -- Bissell, Mina J -- Garcia, Benjamin A -- Kang, Yibin -- Rajasekhar, Vinagolu K -- Ghajar, Cyrus M -- Matei, Irina -- Peinado, Hector -- Bromberg, Jacqueline -- Lyden, David -- R01 CA169416/CA/NCI NIH HHS/ -- R01-CA169416/CA/NCI NIH HHS/ -- U01 CA169538/CA/NCI NIH HHS/ -- U01-CA169538/CA/NCI NIH HHS/ -- England -- Nature. 2015 Nov 19;527(7578):329-35. doi: 10.1038/nature15756. Epub 2015 Oct 28.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Children's Cancer and Blood Foundation Laboratories, Departments of Pediatrics, and Cell and Developmental Biology, Drukier Institute for Children's Health, Meyer Cancer Center, Weill Cornell Medicine, New York, New York 10021, USA. ; Department of Plant Pathology and Microbiology and Center for Biotechnology, National Taiwan University, Taipei 10617, Taiwan. ; Graduate Program in Areas of Basic and Applied Biology, Abel Salazar Biomedical Sciences Institute, University of Porto, 4099-003 Porto, Portugal. ; Department of Obstetrics and Gynecology, Faculty of Medicine, University of Tokyo, Tokyo 113-8655, Japan. ; Proteomics Resource Center, The Rockefeller University, New York, New York 10065, USA. ; Department of Pathology, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Oncology and Pathology, Karolinska Institutet, 17176 Stockholm, Sweden. ; Electron Microscopy Resource Center (EMRC), Rockefeller University, New York, New York 10065, USA. ; Breast Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York, 10065, USA. ; Department of Surgery, County Council of Ostergotland, and Department of Clinical and Experimental Medicine, Faculty of Health Sciences, Linkoping University, 58185 Linkoping, Sweden. ; Life Sciences Division, Lawrence Berkeley National Laboratory, Berkeley, California 94720, USA. ; Genomics Resources Core Facility, Weill Cornell Medicine, New York, New York 10021, USA. ; Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Pediatrics, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Division of Pediatric Oncology, Alberta Children's Hospital, Calgary, Alberta T3B 6A8, Canada. ; Division of Hematology/Oncology, Columbia University School of Medicine, New York, New York 10032, USA. ; Orthopaedic Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Hepato-Pancreato-Biliary Surgery, Oslo University Hospital, Nydalen, Oslo 0424, Norway. ; Department of Cancer Genetics, Institute for Cancer Research, Oslo University Hospital, Nydalen, Oslo 0424, Norway. ; Eppley Institute for Research in Cancer and Allied Diseases, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA. ; Department of Biochemistry and Molecular Biology, University of Nebraska Medical Center, Omaha, Nebraska 68198, USA. ; Gastric and Mixed Tumor Service, Department of Surgery, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Tumor Biology, Norwegian Radium Hospital, Oslo University Hospital, Nydalen, Oslo 0424, Norway. ; Institute for Clinical Medicine, Faculty of Medicine, University of Oslo, Blindern, Oslo 0318, Norway. ; Department of Gynecology, University Medical Center, Martinistrasse 52, 20246 Hamburg, Germany. ; Department of Tumor Biology, University Medical Center Hamburg-Eppendorf, Martinistrasse 52, 20246 Hamburg, Germany. ; Department of Radiation Oncology, Abramson Family Cancer Research Institute, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Department of Biochemistry and Biophysics, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania 19104, USA. ; Department of Molecular Biology, Princeton University, Princeton, New Jersey 08544, USA. ; Rutgers Cancer Institute of New Jersey, New Brunswick, New Jersey 08903, USA. ; Breast Medicine Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. ; Microenvironment and Metastasis Laboratory, Department of Molecular Oncology, Spanish National Cancer Research Center (CNIO), Madrid 28029, Spain. ; Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Department of Medicine, Weill Cornell Medicine, New York, New York 10021, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26524530" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/metabolism ; Brain/cytology/*metabolism ; Cell Line, Tumor ; Endothelial Cells/cytology/metabolism ; Epithelial Cells/cytology/metabolism ; Exosomes/*metabolism ; Female ; Fibroblasts/cytology/metabolism ; Genes, src ; Humans ; Integrin alpha6beta1/metabolism ; Integrin alpha6beta4/antagonists & inhibitors/metabolism ; Integrin beta Chains/metabolism ; Integrin beta4/metabolism ; Integrins/antagonists & inhibitors/*metabolism ; Kupffer Cells/cytology/metabolism ; Liver/cytology/*metabolism ; Lung/cytology/*metabolism ; Mice ; Mice, Inbred C57BL ; Neoplasm Metastasis/*pathology/*prevention & control ; Organ Specificity ; Phosphorylation ; Receptors, Vitronectin/antagonists & inhibitors/metabolism ; S100 Proteins/genetics ; *Tropism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Signalling thresholds and negative B-cell selection in acute lymphoblastic leukaemia (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-03-25
    Description: B cells are selected for an intermediate level of B-cell antigen receptor (BCR) signalling strength: attenuation below minimum (for example, non-functional BCR) or hyperactivation above maximum (for example, self-reactive BCR) thresholds of signalling strength causes negative selection. In approximately 25% of cases, acute lymphoblastic leukaemia (ALL) cells carry the oncogenic BCR-ABL1 tyrosine kinase (Philadelphia chromosome positive), which mimics constitutively active pre-BCR signalling. Current therapeutic approaches are largely focused on the development of more potent tyrosine kinase inhibitors to suppress oncogenic signalling below a minimum threshold for survival. We tested the hypothesis that targeted hyperactivation--above a maximum threshold--will engage a deletional checkpoint for removal of self-reactive B cells and selectively kill ALL cells. Here we find, by testing various components of proximal pre-BCR signalling in mouse BCR-ABL1 cells, that an incremental increase of Syk tyrosine kinase activity was required and sufficient to induce cell death. Hyperactive Syk was functionally equivalent to acute activation of a self-reactive BCR on ALL cells. Despite oncogenic transformation, this basic mechanism of negative selection was still functional in ALL cells. Unlike normal pre-B cells, patient-derived ALL cells express the inhibitory receptors PECAM1, CD300A and LAIR1 at high levels. Genetic studies revealed that Pecam1, Cd300a and Lair1 are critical to calibrate oncogenic signalling strength through recruitment of the inhibitory phosphatases Ptpn6 (ref. 7) and Inpp5d (ref. 8). Using a novel small-molecule inhibitor of INPP5D (also known as SHIP1), we demonstrated that pharmacological hyperactivation of SYK and engagement of negative B-cell selection represents a promising new strategy to overcome drug resistance in human ALL.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441554/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4441554/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Chen, Zhengshan -- Shojaee, Seyedmehdi -- Buchner, Maike -- Geng, Huimin -- Lee, Jae Woong -- Klemm, Lars -- Titz, Bjorn -- Graeber, Thomas G -- Park, Eugene -- Tan, Ying Xim -- Satterthwaite, Anne -- Paietta, Elisabeth -- Hunger, Stephen P -- Willman, Cheryl L -- Melnick, Ari -- Loh, Mignon L -- Jung, Jae U -- Coligan, John E -- Bolland, Silvia -- Mak, Tak W -- Limnander, Andre -- Jumaa, Hassan -- Reth, Michael -- Weiss, Arthur -- Lowell, Clifford A -- Muschen, Markus -- 101880/Wellcome Trust/United Kingdom -- CA180794/CA/NCI NIH HHS/ -- CA180820/CA/NCI NIH HHS/ -- R01 AI068150/AI/NIAID NIH HHS/ -- R01 AI113272/AI/NIAID NIH HHS/ -- R01 CA137060/CA/NCI NIH HHS/ -- R01 CA139032/CA/NCI NIH HHS/ -- R01 CA157644/CA/NCI NIH HHS/ -- R01 CA169458/CA/NCI NIH HHS/ -- R01 CA172558/CA/NCI NIH HHS/ -- R01CA137060/CA/NCI NIH HHS/ -- R01CA139032/CA/NCI NIH HHS/ -- R01CA157644/CA/NCI NIH HHS/ -- R01CA169458/CA/NCI NIH HHS/ -- R01CA172558/CA/NCI NIH HHS/ -- U01 CA157937/CA/NCI NIH HHS/ -- U10 CA180794/CA/NCI NIH HHS/ -- U10 CA180820/CA/NCI NIH HHS/ -- U10 CA180827/CA/NCI NIH HHS/ -- U10 CA180886/CA/NCI NIH HHS/ -- U24 CA114737/CA/NCI NIH HHS/ -- U24 CA196172/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2015 May 21;521(7552):357-61. doi: 10.1038/nature14231. Epub 2015 Mar 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Laboratory Medicine, University of California, San Francisco, California 94143, USA. ; Crump Institute for Molecular Imaging, Department of Molecular and Medical Pharmacology, University of California, Los Angeles, California 90095, USA. ; Rosalind Russell-Ephraim P. Engleman Medical Research Center for Arthritis, Division of Rheumatology, Department of Medicine, Howard Hughes Medical Institute, University of California, San Francisco, California 94143, USA. ; Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, Texas 75390, USA. ; Department of Medicine, Albert Einstein College of Medicine, Bronx, New York 10466, USA. ; Division of Pediatric Oncology and Center for Childhood Cancer Research, Children's Hospital of Philadelphia, Philadelphia, Philadelphia 19104, USA. ; University of New Mexico Cancer Center, Albuquerque, New Mexico 87102, USA. ; Departments of Medicine and Pharmacology, Weill Cornell Medical College, New York, New York 10065, USA. ; Pediatric Hematology-Oncology, University of California, San Francisco, California 94143, USA. ; Department of Molecular Microbiology and Immunology, University of Southern California, Los Angeles, California 90033, USA. ; Receptor Cell Biology Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852, USA. ; Autoimmunity and Functional Genomics Section, Laboratory of Immunogenetics, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 20852, USA. ; The Campbell Family Institute for Breast Cancer Research, University Health Network, 620 University Avenue, Toronto, Ontario M5G 2M9, Canada. ; Department of Anatomy, University of California, San Francisco, California 94143, USA. ; Institute of Immunology, University Clinics Ulm, 89081 Ulm, Germany. ; BIOSS Centre for Biological Signalling Studies and Faculty of Biology, Albert-Ludwigs-Universitat Freiburg, and MPI of Immunbiologie and Epigenetics, 79104 Freiburg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25799995" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Motifs/genetics ; Animals ; Antigens, CD/metabolism ; Antigens, CD31/metabolism ; B-Lymphocytes/drug effects/*metabolism/*pathology ; Cell Death/drug effects ; Cell Line, Tumor ; Cell Transformation, Neoplastic ; Disease Models, Animal ; Drug Resistance, Neoplasm/drug effects ; Enzyme Activation/drug effects ; Female ; Fusion Proteins, bcr-abl/genetics ; Gene Deletion ; Humans ; Intracellular Signaling Peptides and Proteins/agonists/metabolism ; Mice ; Mice, Inbred NOD ; Mice, SCID ; Phosphoric Monoester Hydrolases/antagonists & inhibitors/metabolism ; Precursor Cell Lymphoblastic Leukemia-Lymphoma/drug ; therapy/genetics/*metabolism/*pathology ; Precursor Cells, B-Lymphoid/drug effects/metabolism/pathology ; Protein Tyrosine Phosphatase, Non-Receptor Type 6/deficiency/genetics/metabolism ; Protein-Tyrosine Kinases/metabolism ; Receptors, Antigen, B-Cell/deficiency/genetics/metabolism ; Receptors, Immunologic/genetics/metabolism ; *Signal Transduction/drug effects ; Tyrosine/metabolism ; Xenograft Model Antitumor Assays
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    Microbial community assembly and metabolic function during mammalian corpse decomposition (2015)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2015-12-15
    Description: Vertebrate corpse decomposition provides an important stage in nutrient cycling in most terrestrial habitats, yet microbially mediated processes are poorly understood. Here we combine deep microbial community characterization, community-level metabolic reconstruction, and soil biogeochemical assessment to understand the principles governing microbial community assembly during decomposition of mouse and human corpses on different soil substrates. We find a suite of bacterial and fungal groups that contribute to nitrogen cycling and a reproducible network of decomposers that emerge on predictable time scales. Our results show that this decomposer community is derived primarily from bulk soil, but key decomposers are ubiquitous in low abundance. Soil type was not a dominant factor driving community development, and the process of decomposition is sufficiently reproducible to offer new opportunities for forensic investigations.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Metcalf, Jessica L -- Xu, Zhenjiang Zech -- Weiss, Sophie -- Lax, Simon -- Van Treuren, Will -- Hyde, Embriette R -- Song, Se Jin -- Amir, Amnon -- Larsen, Peter -- Sangwan, Naseer -- Haarmann, Daniel -- Humphrey, Greg C -- Ackermann, Gail -- Thompson, Luke R -- Lauber, Christian -- Bibat, Alexander -- Nicholas, Catherine -- Gebert, Matthew J -- Petrosino, Joseph F -- Reed, Sasha C -- Gilbert, Jack A -- Lynne, Aaron M -- Bucheli, Sibyl R -- Carter, David O -- Knight, Rob -- 3 R01 HG004872-03S2/HG/NHGRI NIH HHS/ -- 5 U01 HG004866-04/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):158-62. doi: 10.1126/science.aad2646. Epub 2015 Dec 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Ecology and Evolutionary Biology, University of Colorado, Boulder, CO 80309, USA. Department of Pediatrics, University of California, San Diego, San Diego, CA 92037, USA. robknight@ucsd.edu jessica.metcalf@colorado.edu. ; Department of Pediatrics, University of California, San Diego, San Diego, CA 92037, USA. ; Department of Chemical and Biological Engineering, University of Colorado, Boulder, CO 80303, USA. ; Department of Ecology and Evolution, University of Chicago, 1101 East 57th Street, Chicago, IL 60637, USA. Institute for Genomic and Systems Biology, University of Chicago, 900 East 57th Street, Chicago, IL 606037, USA. ; Department of Microbiology and Immunology, Stanford University, Stanford, CA 94305, USA. ; Department of Ecology and Evolutionary Biology, University of Colorado, Boulder, CO 80309, USA. Department of Pediatrics, University of California, San Diego, San Diego, CA 92037, USA. ; Department of Ecology and Evolution, University of Chicago, 1101 East 57th Street, Chicago, IL 60637, USA. Biosciences Division, Argonne National Laboratory, South Cass Avenue, Argonne, IL 60439, USA. ; Department of Ecology and Evolution, University of Chicago, 1101 East 57th Street, Chicago, IL 60637, USA. Biosciences Division, Argonne National Laboratory, South Cass Avenue, Argonne, IL 60439, USA. Department of Surgery, University of Chicago, A27 South Maryland Avenue, Chicago, IL 60637, USA. ; Department of Biological Sciences, Sam Houston State University, Huntsville, TX 77340, USA. ; Nestle Institute of Health Sciences, Ecole Polytechnique Federale Lausanne, Batiment H, 1015 Lausanne, Switzerland. ; BioFrontiers Institute, University of Colorado, Boulder, CO 80303, USA. ; Alkek Center for Metagenomics and Microbiome Research, Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030, USA. ; U.S. Geological Survey, Southwest Biological Science Center, Moab, UT 84532, USA. ; Department of Ecology and Evolution, University of Chicago, 1101 East 57th Street, Chicago, IL 60637, USA. Institute for Genomic and Systems Biology, University of Chicago, 900 East 57th Street, Chicago, IL 606037, USA. Biosciences Division, Argonne National Laboratory, South Cass Avenue, Argonne, IL 60439, USA. Department of Surgery, University of Chicago, A27 South Maryland Avenue, Chicago, IL 60637, USA. Marine Biological Laboratory, 7 MBL St, Woods Hole, MA 02543, USA. ; Laboratory of Forensic Taphonomy, Forensic Sciences Unit, Division of Natural Sciences and Mathematics, Chaminade University of Honolulu, Honolulu, HI 96816, USA. ; Department of Pediatrics, University of California, San Diego, San Diego, CA 92037, USA. Department of Computer Science and Engineering, University of California, San Diego, San Diego, CA 92037, USA. robknight@ucsd.edu jessica.metcalf@colorado.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26657285" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bacteria/classification/*metabolism ; Biodegradation, Environmental ; *Cadaver ; Ecosystem ; Fungi/classification/*metabolism ; Mice ; *Microbial Consortia ; Nitrogen Cycle ; Soil/chemistry/classification ; *Soil Microbiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 6
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    Presenting the epigenome roadmap (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-02-20
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Skipper, Magdalena -- Eccleston, Alex -- Gray, Noah -- Heemels, Therese -- Le Bot, Nathalie -- Marte, Barbara -- Weiss, Ursula -- England -- Nature. 2015 Feb 19;518(7539):313. doi: 10.1038/518313a.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25693561" target="_blank"〉PubMed〈/a〉
    Keywords: Alzheimer Disease/genetics ; Animals ; Autoimmune Diseases/genetics ; Cell Differentiation/genetics ; Chromatin Assembly and Disassembly/genetics ; DNA Methylation/genetics ; Epigenesis, Genetic/*genetics ; *Epigenomics ; Genome, Human/genetics ; Haplotypes/genetics ; Histones/metabolism ; Humans ; Mice ; Neoplasms/genetics ; Stem Cells/cytology/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
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    Brain tumour cells interconnect to a functional and resistant network (2015)
    Nature Publishing Group (NPG)
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    Publication Date: 2015-11-05
    Description: Astrocytic brain tumours, including glioblastomas, are incurable neoplasms characterized by diffusely infiltrative growth. Here we show that many tumour cells in astrocytomas extend ultra-long membrane protrusions, and use these distinct tumour microtubes as routes for brain invasion, proliferation, and to interconnect over long distances. The resulting network allows multicellular communication through microtube-associated gap junctions. When damage to the network occurred, tumour microtubes were used for repair. Moreover, the microtube-connected astrocytoma cells, but not those remaining unconnected throughout tumour progression, were protected from cell death inflicted by radiotherapy. The neuronal growth-associated protein 43 was important for microtube formation and function, and drove microtube-dependent tumour cell invasion, proliferation, interconnection, and radioresistance. Oligodendroglial brain tumours were deficient in this mechanism. In summary, astrocytomas can develop functional multicellular network structures. Disconnection of astrocytoma cells by targeting their tumour microtubes emerges as a new principle to reduce the treatment resistance of this disease.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Osswald, Matthias -- Jung, Erik -- Sahm, Felix -- Solecki, Gergely -- Venkataramani, Varun -- Blaes, Jonas -- Weil, Sophie -- Horstmann, Heinz -- Wiestler, Benedikt -- Syed, Mustafa -- Huang, Lulu -- Ratliff, Miriam -- Karimian Jazi, Kianush -- Kurz, Felix T -- Schmenger, Torsten -- Lemke, Dieter -- Gommel, Miriam -- Pauli, Martin -- Liao, Yunxiang -- Haring, Peter -- Pusch, Stefan -- Herl, Verena -- Steinhauser, Christian -- Krunic, Damir -- Jarahian, Mostafa -- Miletic, Hrvoje -- Berghoff, Anna S -- Griesbeck, Oliver -- Kalamakis, Georgios -- Garaschuk, Olga -- Preusser, Matthias -- Weiss, Samuel -- Liu, Haikun -- Heiland, Sabine -- Platten, Michael -- Huber, Peter E -- Kuner, Thomas -- von Deimling, Andreas -- Wick, Wolfgang -- Winkler, Frank -- England -- Nature. 2015 Dec 3;528(7580):93-8. doi: 10.1038/nature16071. Epub 2015 Nov 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurology Clinic and National Center for Tumor Diseases, University Hospital Heidelberg, INF 400, 69120 Heidelberg, Germany. ; Clinical Cooperation Unit Neurooncology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ; Department of Neuropathology, Institute of Pathology, Ruprecht-Karls University Heidelberg, INF 224, 69120 Heidelberg, Germany. ; Clinical Cooperation Unit Neuropathology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), INF 224, 69120 Heidelberg, Germany. ; Department of Functional Neuroanatomy, Institute of Anatomy and Cell Biology, Heidelberg University, INF 307, 69120 Heidelberg, Germany. ; Department of Diagnostic and Interventional Neuroradiology, Klinikum rechts der Isar der Technischen Universitat Munchen, 81675 Munich, Germany. ; Neurosurgery Clinic, University Hospital Heidelberg, INF 400, 69120 Heidelberg, Germany. ; Department of Neuroradiology, University Hospital Heidelberg, INF 400, 69120 Heidelberg, Germany. ; Department of Neurophysiology, Institute of Physiology, University of Wurzburg, 97070 Wurzburg, Germany. ; Department of Medical Physics, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ; Institute of Cellular Neurosciences, Medical Faculty, University of Bonn, Sigmund-Freud-Strasse 25, 53105 Bonn, Germany. ; Light Microscopy Facility, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ; Department of Translational Immunology, German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ; Department of Biomedicine, University of Bergen, Jonas Lies vei 91, 5009 Bergen, Norway. ; Institute of Neurology, Medical University of Vienna, Vienna, Austria; Comprehensive Cancer Center, CNS Unit, Medical University of Vienna, 1090 Vienna, Austria. ; Tools For Bio-Imaging, Max-Planck-Institute of Neurobiology, 82152 Martinsried, Germany. ; Institute of Physiology II, Eberhard Karls University of Tubingen, 72074 Tubingen, Germany. ; Department of Medicine I, Medical University of Vienna, Vienna, Austria; Comprehensive Cancer Center, CNS Unit, Medical University of Vienna, 1090 Vienna, Austria. ; Hotchkiss Brain Institute, Faculty of Medicine, University of Calgary, Calgary, Alberta T2N 4N1, Canada. ; Department of Cell Biology and Anatomy, Faculty of Medicine, University of Calgary, Calgary, Alberta T2N 4Z6, Canada. ; Clark Smith Brain Tumor Research Centre, Southern Alberta Cancer Research Institute, Faculty of Medicine, University of Calgary, Calgary, Alberta, T2N 4N1, Canada. ; Helmholtz Young Investigator Group, Normal and Neoplastic CNS Stem Cells, DKFZ-ZMBH Alliance, German Cancer Research Center (DKFZ), INF 280, 69120 Heidelberg, Germany. ; Clinical Cooperation Unit Neuroimmunology and Brain Tumor Immunology, German Cancer Consortium (DKTK), German Cancer Research Center (DKFZ), 69120 Heidelberg, Germany. ; CCU Molecular and Radiation Oncology, German Cancer Research Center (DKFZ), INF 280, 69120 Heidelberg, Germany. ; Department of Radiation Oncology, University Hospital Heidelberg, 69120 Heidelberg, Germany.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26536111" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Astrocytoma/metabolism/*pathology/radiotherapy ; Brain Neoplasms/metabolism/*pathology/radiotherapy ; Cell Communication/radiation effects ; Cell Death/radiation effects ; Cell Proliferation/radiation effects ; Cell Surface Extensions/metabolism/radiation effects ; Cell Survival/radiation effects ; Connexin 43/metabolism ; Disease Progression ; GAP-43 Protein/metabolism ; Gap Junctions/*metabolism/radiation effects ; Glioma/metabolism/pathology/radiotherapy ; Humans ; Male ; Mice ; Mice, Nude ; Neoplasm Invasiveness ; Radiation Tolerance/drug effects
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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