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  • 1.
    Adolfsson, J
    et al.
    Lund University.
    Månsson, R
    Lund University.
    Buza-Vidas, N
    Lund University.
    Hultquist, A
    Lund University.
    Liuba, K
    Lund University.
    Jensen, C T
    Lund University.
    Bryder, D
    Lund University.
    Yang, L
    Lund University.
    Borge, O-J
    Lund University.
    Thoren, L A M
    Lund University.
    Anderson, K
    Lund University.
    Sitnicka, E
    Lund University.
    Sasaki, Y
    Lund University.
    Sigvardsson, Mikael
    Lund University.
    Jacobsen, S E W
    Lund University.
    Identification of Flt3(+) lympho-myeloid stem cells lacking erythro-megakaryocytic potential: A revised road map for adult blood lineage commitment2005Inngår i: Cell, ISSN 0092-8674, E-ISSN 1097-4172, Vol. 121, nr 2, s. 295-306Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    All blood cell lineages derive from a common hematopoietic stem cell (HSC). The current model implicates that the first lineage commitment step of adult pluripotent HSCs results in a strict separation into common lymphoid and common myeloid precursors. We present evidence for a population of cells which, although sustaining a high proliferative and combined lympho-myeloid differentiation potential, have lost the ability to adopt erythroid and megakaryocyte lineage fates. Cells in the Lin-Sca-1+c-kit+ HSC compartment coexpressing high levels of the tyrosine kinase receptor Flt3 sustain granulocyte, monocyte, and B and T cell potentials but in contrast to Lin-Sca-1(+)ckit(+)Flt3(-) HSCs fail to produce significant erythroid and megakaryocytic progeny. This distinct lineage restriction site is accompanied by downregulation of genes for regulators of erythroid and megakaryocyte development. In agreement with representing a lymphoid primed progenitor, Lin(-)Sca-l(+)c-kit(+)CD34(+)Flt3(+) cells display upregulated IL-7 receptor gene expression. Based on these observations, we propose a revised road map for adult blood lineage development.

  • 2.
    Allan, Douglas W
    et al.
    Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115 USA.
    St Pierre, Susan E
    Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115 USA.
    Miguel-Aliaga, Irene
    Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115 USA.
    Thor, Stefan
    Department of Neurobiology, Harvard Medical School, 220 Longwood Avenue, Boston, MA 02115 USA.
    Specification of Neuropeptide Cell Identity by the Integration of Retrograde BMP Signaling and a Combinatorial Transcription Factor Code2003Inngår i: Cell, ISSN 0092-8674, E-ISSN 1097-4172, Vol. 113, nr 1, s. 73-86Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Individual neurons express only one or a few of the many identified neurotransmitters and neuropeptides, but the molecular mechanisms controlling their selection are poorly understood. In the Drosophila ventral nerve cord, the six Tv neurons express the neuropeptide gene FMRFamide. Each Tv neuron resides within a neuronal cell group specified by the LIM-homeodomain gene apterous. We find that the zinc-finger gene squeeze acts in Tv cells to promote their unique axon pathfinding to a peripheral target. There, the BMP ligand Glass bottom boat activates the Wishful thinking receptor, initiating a retrograde BMP signal in the Tv neuron. This signal acts together with apterous and squeeze to activate FMRFamide expression. Reconstituting this "code," by combined BMP activation and apterous/squeeze misexpression, triggers ectopic FMRFamide expression in peptidergic neurons. Thus, an intrinsic transcription factor code integrates with an extrinsic retrograde signal to select a specific neuropeptide identity within peptidergic cells.

  • 3.
    Baumgardt, Magnus
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Utvecklingsbiologi. Linköpings universitet, Hälsouniversitetet.
    Karlsson, Daniel
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Utvecklingsbiologi. Linköpings universitet, Hälsouniversitetet.
    Terriente, Javier
    Division of Developmental Neuroscience, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, United Kingdom.
    Díaz-Benjumea, Fernando J.
    Centro de Biología Molecular-Severo Ochoa/C.S.I.C., Universidad Autónoma-Cantoblanco, Madrid 28049, Spain.
    Thor, Stefan
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Utvecklingsbiologi. Linköpings universitet, Hälsouniversitetet.
    Neuronal Subtype Specification within a Lineage by Opposing Temporal Feed-Forward Loops2009Inngår i: Cell, ISSN 0092-8674, E-ISSN 1097-4172, Vol. 139, nr 5, s. 969-982Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Neural progenitors generate distinct cell types at different stages, but the mechanisms controlling these temporal transitions are poorly understood. In the Drosophila CNS, a cascade of transcription factors, the ‘temporal gene cascade’, has been identified, that acts to alter progenitor competence over time. However, many CNS lineages display broad temporal windows, and it is unclear how broad windows progress into sub-windows that generate unique cell types. We have addressed this issue in an identifiable Drosophila CNS lineage, and find that a broad castor temporal window is sub-divided by two different feed-forward loops, both of which are triggered by castor itself. The first loop acts to specify a unique cell fate, while the second loop suppresses the first loop, thereby allowing for the generation of alternate cell fates. This mechanism of temporal and ‘sub-temporal’ genes acting in opposing feed-forward loops may be used by many stem cell lineages to generate diversity.

  • 4.
    Guzzi, Nicola
    et al.
    Lund Univ, Sweden.
    Ciesla, Maciej
    Lund Univ, Sweden.
    Thi Ngoc, Phuong Cao
    Lund Univ, Sweden.
    Lang, Stefan
    Lund Univ, Sweden.
    Arora, Sonali
    Univ Washington, WA 98195 USA.
    Dimitriou, Marios
    Karolinska Inst, Sweden.
    Pimkova, Kristyna
    Lund Univ, Sweden.
    Sommarin, Mikael N. E.
    Lund Univ, Sweden.
    Munita, Roberto
    Lund Univ, Sweden.
    Lubas, Michal
    Univ Copenhagen, Denmark.
    Lim, Yiting
    Univ Washington, WA 98195 USA.
    Okuyama, Kazuki
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten.
    Soneji, Shamit
    Lund Univ, Sweden.
    Karlsson, Goran
    Lund Univ, Sweden.
    Hansson, Jenny
    Lund Univ, Sweden.
    Jonsson, Goran
    Lund Univ, Sweden.
    Lund, Anders H.
    Univ Copenhagen, Denmark.
    Sigvardsson, Mikael
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för mikrobiologi och molekylär medicin. Linköpings universitet, Medicinska fakulteten. Lund Univ, Sweden.
    Hellstrom-Lindberg, Eva
    Karolinska Inst, Sweden.
    Hsieh, Andrew C.
    Univ Washington, WA 98195 USA.
    Bellodi, Cristian
    Lund Univ, Sweden.
    Pseudouridylation of tRNA-Derived Fragments Steers Translational Control in Stem Cells2018Inngår i: Cell, ISSN 0092-8674, E-ISSN 1097-4172, Vol. 173, nr 5, s. 1204-+Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Pseudouridylation (J) is the most abundant and widespread type of RNA epigenetic modification in living organisms; however, the biological role of J remains poorly understood. Here, we show that a J-driven posttranscriptional program steers translation control to impact stem cell commitment during early embryogenesis. Mechanistically, the J "writer PUS7 modifies and activates a novel network of tRNA-derived small fragments (tRFs) targeting the translation initiation complex. PUS7 inactivation in embryonic stem cells impairs tRF-mediated translation regulation, leading to increased protein biosynthesis and defective germ layer specification. Remarkably, dysregulation of this posttranscriptional regulatory circuitry impairs hematopoietic stem cell commitment and is common to aggressive subtypes of human myelodysplastic syndromes. Our findings unveil a critical function of J in directing translation control in stem cells with important implications for development and disease.

  • 5.
    Koch, Stefan
    et al.
    Division of Molecular Embryology, DKFZ-ZMBH Alliance, Heidelberg, Germany.
    Acebron, Sergio P.
    Division of Molecular Embryology, DKFZ-ZMBH Alliance, Heidelberg, Germany.
    Herbst, Jessica
    Division of Molecular Embryology, DKFZ-ZMBH Alliance, Heidelberg, Germany.
    Hatiboglu, Gencay
    Department of Urology, University of Heidelberg, Heidelberg, Germany.
    Niehrs, Christof
    Division of Molecular Embryology, DKFZ-ZMBH Alliance, Heidelberg, Germany; Institute of Molecular Biology (IMB), Mainz, Germany.
    Post-transcriptional Wnt Signaling Governs Epididymal Sperm Maturation2015Inngår i: Cell, ISSN 0092-8674, E-ISSN 1097-4172, Vol. 163, nr 5, s. 1225-1236Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The canonical Wnt signaling pathway is of paramount importance in development and disease. An emergent question is whether the upstream cascade of the canonical Wnt pathway has physiologically relevant roles beyond beta-catenin-mediated transcription, which is difficult to study due to the pervasive role of this protein. Here, we show that transcriptionally silent spermatozoa respond to Wnt signals released from the epididymis and that mice mutant for the Wnt regulator Cyclin Y-like 1 are male sterile due to immotile and malformed spermatozoa. Post-transcriptional Wnt signaling impacts spermatozoa through GSK3 by (1) reducing global protein poly-ubiquitination to maintain protein homeostasis; (2) inhibiting septin 4 phosphorylation to establish a membrane diffusion barrier in the sperm tail; and (3) inhibiting protein phosphatase 1 to initiate sperm motility. The results indicate that Wnt signaling orchestrates a rich post-transcriptional sperm maturation program and invite revisiting transcription-independent Wnt signaling in somatic cells as well.

  • 6.
    Link, Verena M
    et al.
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA; Faculty of Biology, Division of Evolutionary Biology, Ludwig-Maximilian University of Munich, Munich, Germany.
    Duttke, Sascha H
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
    Chun, Hyun B
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
    Holtman, Inge R
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA; Department of Neuroscience, Section Medical Physiology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
    Westin, Emma
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
    Hoeksema, Marten A
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
    Abe, Yohei
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
    Skola, Dylan
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
    Romanoski, Casey E
    Department of Cellular and Molecular Medicine, University of Arizona, Tucson, AZ, USA.
    Tao, Jenhan
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
    Fonseca, Gregory J
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
    Troutman, Ty D
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
    Spann, Nathanael J
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
    Strid, Tobias
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
    Sakai, Mashito
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA.
    Yu, Miao
    Ludwig Institute for Cancer Research, La Jolla, CA, USA.
    Hu, Rong
    Ludwig Institute for Cancer Research, La Jolla, CA, USA.
    Fang, Rongxin
    Ludwig Institute for Cancer Research, La Jolla, CA, USA.
    Metzler, Dirk
    Faculty of Biology, Division of Evolutionary Biology, Ludwig-Maximilian University of Munich, Munich, Germany.
    Ren, Bing
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA; Ludwig Institute for Cancer Research, La Jolla, CA, USA.
    Glass, Christopher K
    Department of Cellular and Molecular Medicine, School of Medicine, University of California, San Diego, La Jolla, CA, USA; Department of Medicine, University of California, San Diego, La Jolla, CA, USA.
    Analysis of Genetically Diverse Macrophages Reveals Local and Domain-wide Mechanisms that Control Transcription Factor Binding and Function.2018Inngår i: Cell, ISSN 0092-8674, E-ISSN 1097-4172, Vol. 173, nr 7, s. 1796-1809.e17, artikkel-id S0092-8674(18)30511-7Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Non-coding genetic variation is a major driver of phenotypic diversity and allows the investigation of mechanisms that control gene expression. Here, we systematically investigated the effects of >50 million variations from five strains of mice on mRNA, nascent transcription, transcription start sites, and transcription factor binding in resting and activated macrophages. We observed substantial differences associated with distinct molecular pathways. Evaluating genetic variation provided evidence for roles of ∼100 TFs in shaping lineage-determining factor binding. Unexpectedly, a substantial fraction of strain-specific factor binding could not be explained by local mutations. Integration of genomic features with chromatin interaction data provided evidence for hundreds of connected cis-regulatory domains associated with differences in transcription factor binding and gene expression. This system and the >250 datasets establish a substantial new resource for investigation of how genetic variation affects cellular phenotypes.

  • 7.
    Mogilenko, Denis A.
    et al.
    Univ Lille, France.
    Haas, Joel T.
    Univ Lille, France.
    Lhomme, Laurent
    Univ Lille, France.
    Fleury, Sebastien
    Univ Lille, France.
    Quemener, Sandrine
    Univ Lille, France.
    Levavasseur, Matthieu
    Univ Lille, France; CHU Lille, France.
    Becquart, Coralie
    Univ Lille, France; CHU Lille, France.
    Wartelle, Julien
    Univ Lille, France.
    Bogomolova, Alexandra
    Univ Lille, France.
    Pineau, Laurent
    Univ Lille, France.
    Molendi-Coste, Olivier
    Univ Lille, France.
    Lancel, Steve
    Univ Lille, France.
    Dehondt, Helene
    Univ Lille, France.
    Gheeraert, Celine
    Univ Lille, France.
    Melchior, Aurelie
    Univ Lille, France.
    Dewas, Cedric
    Univ Lille, France.
    Nikitin, Artemii
    Univ Lille, France.
    Pic, Samuel
    Univ Lille, France.
    Rabhi, Nabil
    Univ Lille, France.
    Annicotte, Jean-Sebastien
    Univ Lille, France.
    Oyadomari, Seiichi
    Tokushima Univ, Japan.
    Velasco-Hernandez, Talia
    Linköpings universitet, Institutionen för klinisk och experimentell medicin. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Centrum för kirurgi, ortopedi och cancervård, Hematologiska kliniken US.
    Cammenga, Jörg
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för Kirurgi, Ortopedi och Onkologi. Linköpings universitet, Medicinska fakulteten. Region Östergötland, Centrum för kirurgi, ortopedi och cancervård, Hematologiska kliniken US.
    Foretz, Marc
    Univ Paris 05, France; Inst Cochin, France; CNRS, France.
    Viollet, Benoit
    Univ Paris 05, France; Inst Cochin, France; CNRS, France.
    Vukovic, Milica
    Queen Mary Univ London, England.
    Villacreces, Arnaud
    Queen Mary Univ London, England.
    Kranc, Kamil
    Queen Mary Univ London, England.
    Carmeliet, Peter
    VIB, Belgium; Univ Leuven, Belgium.
    Marot, Guillemette
    Univ Lille, France.
    Boulter, Alexis
    Univ Florida, FL 32610 USA.
    Tavernier, Simon
    Univ Ghent, Belgium; Univ Ghent, Belgium.
    Berod, Luciana
    TWINCORE, Germany.
    Longhi, Maria P.
    Queen Mary Univ London, England.
    Paget, Christophe
    Univ Tours, France.
    Janssens, Sophie
    Univ Ghent, Belgium.
    Staumont-Salle, Delphine
    Univ Lille, France; CHU Lille, France.
    Aksoy, Ezra
    Queen Mary Univ London, England.
    Staels, Bart
    Univ Lille, France.
    Dombrowicz, David
    Univ Lille, France.
    Metabolic and Innate Immune Cues Merge into a Specific Inflammatory Response via the UPR2019Inngår i: Cell, ISSN 0092-8674, E-ISSN 1097-4172, Vol. 177, nr 5, s. 1201-Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Innate immune responses are intricately linked with intracellular metabolism of myeloid cells. Toll-like receptor (TLR) stimulation shifts intracellular metabolism toward glycolysis, while anti-inflammatory signals depend on enhanced mitochondrial respiration. How exogenous metabolic signals affect the immune response is unknown. We demonstrate that TLR-dependent responses of dendritic cells (DCs) are exacerbated by a high-fatty-acid (FA) metabolic environment. FAs suppress the TLR-induced hexokinase activity and perturb tricarboxylic acid cycle metabolism. These metabolic changes enhance mitochondria! reactive oxygen species (mtROS) production and, in turn, the unfolded protein response (UPR), leading to a distinct transcriptomic signature with IL-23 as hallmark. Interestingly, chemical or genetic suppression of glycolysis was sufficient to induce this specific immune response. Conversely, reducing mtROS production or DC-specific deficiency in XBP1 attenuated IL-23 expression and skin inflammation in an IL-23-dependent model of psoriasis. Thus, fine-tuning of innate immunity depends on optimization of metabolic demands and minimization of mtROS-induced UPR.

  • 8.
    Pfarr, C. M.
    et al.
    Département des Biotechnologies, Institut Pasteur, Paris, France.
    Mechta, F.
    Département des Biotechnologies, Institut Pasteur, Paris, France.
    Spyrou, Giannis
    Département des Biotechnologies, Institut Pasteur, Paris, France.
    Lallemand, D.
    Département des Biotechnologies, Institut Pasteur, Paris, France.
    Carillo, S.
    Institut de Genetique Moleculaire de Montpellier Unité Mixte de Recherche, Montpellier, France.
    Yaniv, M.
    Département des Biotechnologies, Institut Pasteur, Paris, France.
    Mouse JunD negatively regulates fibroblast growth and antagonizes transformation by ras1994Inngår i: Cell, ISSN 0092-8674, E-ISSN 1097-4172, Vol. 76, nr 4, s. 747-760Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    As NIH 3T3 fibroblasts become quiescent, the level of c-Jun protein decreases while JunD accumulates. When resting cells are stimulated with fresh serum, nuclear-localized JunD is rapidly degraded, followed by resynthesis of both c-Jun and JunD later in G1. Overexpression of JunD results in slower growth and an increase in the percentage of cells in G0/G1 while c-Jun overexpression produces larger S/G2 and M phase populations. In addition, JunD partially suppresses transformation by an activated ras gene whereas c-Jun cooperates with ras to transform cells. These data indicate that two closely related transcription factors can function in an opposing manner.

  • 9.
    Rausenberger, Julia
    et al.
    University of Freiburg.
    Tscheuschler, Anke
    University of Freiburg.
    Nordmeier, Wiebke
    University of Tubingen.
    Wuest, Florian
    University of Freiburg.
    Timmer, Jens
    Linköpings universitet, Hälsouniversitetet. Linköpings universitet, Institutionen för klinisk och experimentell medicin, Cellbiologi.
    Schaefer, Eberhard
    University of Freiburg.
    Fleck, Christian
    University of Freiburg.
    Hiltbrunner, Andreas
    University of Tubingen.
    Photoconversion and Nuclear Trafficking Cycles Determine Phytochrome As Response Profile to Far-Red Light2011Inngår i: Cell, ISSN 0092-8674, E-ISSN 1097-4172, Vol. 146, nr 5, s. 813-825Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Phytochrome A (phyA) is the only photoreceptor in plants, initiating responses in far-red light and, as such, essential for survival in canopy shade. Although the absorption and the ratio of active versus total phyA are maximal in red light, far-red light is the most efficient trigger of phyA-dependent responses. Using a joint experimental-theoretical approach, we unravel the mechanism underlying this shift of the phyA action peak from red to far-red light and show that it relies on specific molecular interactions rather than on intrinsic changes to phyAs spectral properties. According to our model, the dissociation rate of the phyA-FHY1/FHL nuclear import complex is a principle determinant of the phyA action peak. The findings suggest how higher plants acquired the ability to sense far-red light from an ancestral photoreceptor tuned to respond to red light.

  • 10.
    Sekijima, Y.
    et al.
    Department of Chemistry, Skaggs Institute of Chemical Biology, San Diego, CA 92037, United States, Third Department of Medicine, Shinshu University, School of Medicine, 3-1-1 Asahi, Matsumoto 390-8621, Japan.
    Wiseman, R.L.
    Department of Chemistry, Skaggs Institute of Chemical Biology, San Diego, CA 92037, United States.
    Matteson, J.
    Dept. of Molecular and Cell Biology, Inst. Childhood and Neglected Dis., Scripps Research Institute, 10550 N. Torrey Pines Road, San Diego, CA 92037, United States.
    Hammarstrom, P.
    Hammarström, P., Department of Chemistry, Skaggs Institute of Chemical Biology, San Diego, CA 92037, United States, IFM-Department of Chemistry, Linkoping University, 581 83 Linkoping, Sweden.
    Miller, S.R.
    Department of Chemistry, Skaggs Institute of Chemical Biology, San Diego, CA 92037, United States.
    Sawkar, A.R.
    Department of Chemistry, Skaggs Institute of Chemical Biology, San Diego, CA 92037, United States.
    Balch, W.E.
    Dept. of Molecular and Cell Biology, Inst. Childhood and Neglected Dis., Scripps Research Institute, 10550 N. Torrey Pines Road, San Diego, CA 92037, United States.
    Kelly, J.W.
    Department of Chemistry, Skaggs Institute of Chemical Biology, San Diego, CA 92037, United States.
    The biological and chemical basis for tissue-selective amyloid disease2005Inngår i: Cell, ISSN 0092-8674, E-ISSN 1097-4172, Vol. 121, nr 1, s. 73-85Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Factors controlling the onset and progression of extracellular amyloid diseases remain largely unknown. Central to disease etiology is the efficiency of the endoplasmic reticulum (ER) machinery that targets destabilized mutant proteins for degradation and the enhanced tendency of these variants to aggregate if secreted. We demonstrate that mammalian cells secrete numerous transthyretin (TTR) disease-associated variants with wild-type efficiency in spite of compromised folding energetics. Only the most highly destabilized TTR variants are subjected to ER-associated degradation (ERAD) and then only in certain tissues, providing insight into tissue selective amyloidosis. Rather than a "quality control" standard based on wild-type stability, we find that ER-assisted folding (ERAF), based on global protein energetics, determines the extent of export. We propose that ERAF (influenced by the energetics of the protein fold, chaperone enzyme distributions, and metabolite chaperones) in competition with ERAD defines the unique secretory aptitude of each tissue. Copyright ©2005 by Elsevier Inc.

  • 11.
    Sekijima, Y
    et al.
    The Skaggs Institute of Chemical Biology.
    Wiseman, R.L.
    The Skaggs Institute of Chemical Biology.
    Matteson, J
    The Scripps Research Institute.
    Hammarström, Per
    The Skaggs Institute of Chemical Biology.
    Miller, S.R
    The Skaggs Institute of Chemical Biology.
    Balch, W.E
    The Scripps Research Institute.
    Kelly, J.W.
    The Skaggs Institute of Chemical Biology.
    The Biological and Chemical Basis for Tissue Selective Transthyretin Amyloid Disease2005Inngår i: Cell, ISSN 0092-8674, E-ISSN 1097-4172, Vol. 121, nr 1, s. 73-85Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Factors controlling the onset and progression of extracellular amyloid diseases remain largely unknown. Central to disease etiology is the efficiency of the endoplasmic reticulum (ER) machinery that targets destabilized mutant proteins for degradation and the enhanced tendency of these variants to aggregate if secreted. We demonstrate that mammalian cells secrete numerous transthyretin (TTR) disease-associated variants with wild-type efficiency in spite of compromised folding energetics. Only the most highly destabilized TTR variants are subjected to ER-associated degradation (ERAD) and then only in certain tissues, providing insight into tissue selective amyloidosis. Rather than a quality control standard based on wild-type stability, we find that ER-assisted folding (ERAF), based on global protein energetics, determines the extent of export. We propose that ERAF (influenced by the energetics of the protein fold, chaperone enzyme distributions, and metabolite chaperones) in competition with ERAD defines the unique secretory aptitude of each tissue.

  • 12.
    Öst, Anita
    et al.
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Hälsouniversitetet. Max Planck Institute Immunobiol and Epigenet, Germany.
    Lempradl, Adelheid
    Max Planck Institute Immunobiol and Epigenet, Germany.
    Casas, Eduard
    Institute Medical Predict and Personalitzada Canc, Spain; ICO Hospital GermansTrias and Pujol, Spain.
    Weigert, Melanie
    Max Planck Institute Immunobiol and Epigenet, Germany.
    Tiko, Theodor
    Max Planck Institute Immunobiol and Epigenet, Germany.
    Deniz, Merdin
    Max Planck Institute Immunobiol and Epigenet, Germany.
    Pantano, Lorena
    Institute Medical Predict and Personalitzada Canc, Spain.
    Boenisch, Ulrike
    Max Planck Institute Immunobiol and Epigenet, Germany.
    Itskov, Pavel M.
    Champalimaud Centre Unknown, Portugal.
    Stoeckius, Marlon
    Max Delbruck Centre Molecular Med, Germany.
    Ruf, Marius
    Max Planck Institute Immunobiol and Epigenet, Germany.
    Rajewsky, Nikolaus
    Max Delbruck Centre Molecular Med, Germany.
    Reuter, Gunter
    University of Halle Wittenberg, Germany.
    Iovino, Nicola
    Max Planck Institute Immunobiol and Epigenet, Germany.
    Ribeiro, Carlos
    Champalimaud Centre Unknown, Portugal.
    Alenius, Mattias
    Linköpings universitet, Institutionen för klinisk och experimentell medicin, Avdelningen för cellbiologi. Linköpings universitet, Hälsouniversitetet.
    Heyne, Steffen
    Max Planck Institute Immunobiol and Epigenet, Germany.
    Vavouri, Tanya
    Institute Medical Predict and Personalitzada Canc, Spain; ICO Hospital GermansTrias and Pujol, Spain.
    Pospisilik, J. Andrew
    Max Planck Institute Immunobiol and Epigenet, Germany.
    Paternal Diet Defines Offspring Chromatin State and Intergenerational Obesity2014Inngår i: Cell, ISSN 0092-8674, E-ISSN 1097-4172, Vol. 159, nr 6, s. 1352-1364Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    The global rise in obesity has revitalized a search for genetic and epigenetic factors underlying the disease. We present a Drosophila model of paternal-diet-induced intergenerational metabolic reprogramming (IGMR) and identify genes required for its encoding in offspring. Intriguingly, we find that as little as 2 days of dietary intervention in fathers elicits obesity in offspring. Paternal sugar acts as a physiological suppressor of variegation, desilencing chromatin-state-defined domains in both mature sperm and in offspring embryos. We identify requirements for H3K9/K27me3-dependent reprogramming of metabolic genes in two distinct germline and zygotic windows. Critically, we find evidence that a similar system may regulate obesity susceptibility and phenotype variation in mice and humans. The findings provide insight into the mechanisms underlying intergenerational metabolic reprogramming and carry profound implications for our understanding of phenotypic variation and evolution.

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