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REBUILDCNS SIGNED

Redirecting glial progenitor fate to rebuild the injured Brain

Total Cost €

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EC-Contrib. €

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Partnership

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 REBUILDCNS project word cloud

Explore the words cloud of the REBUILDCNS project. It provides you a very rough idea of what is the project "REBUILDCNS" about.

fundamental    preliminary    too    lines    platforms    underlying    exit    leads    excitingly    modulation    competence    follow    function    genomics    rodents    becomes    over    inflammatory    ve    validated    manipulation    cellular    tracing    progenitor    enhancer    experimental    edge    glial    transcriptional    types    rules    underlie    signature    billions    chromatin    indicates    biology    damaged    genome    mechanisms    decisions    connections    brain    restricted    missing    combined    led    identity    breakthroughs    treating    fate    shown    directed    injured    data    functional    transcription    protocols    despite    iuml    million    zebrafish    adult    embryonic    envisage    lineage    governing    discoveries    activation    technological    regenerating    drives    dormant    progenitors    mouse    models    single    transcriptome    repair    demethylation    direct    disorder    landscape    injury    generate    few    impacts    regenerative    activates    diversity    editing    cutting    genetics    endogenous    cell    translational    ways    na    omics    choices    enhancers    attempt    clonal    combining    lab    re    developmental    establishing    epigenome    environment    multidisciplinary    generation    leverage    cns   

Project "REBUILDCNS" data sheet

The following table provides information about the project.

Coordinator
DEUTSCHES KREBSFORSCHUNGSZENTRUM HEIDELBERG 

Organization address
address: IM NEUENHEIMER FELD 280
city: HEIDELBERG
postcode: 69120
website: www.dkfz.de

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Germany [DE]
 Total cost 2˙000˙000 €
 EC max contribution 2˙000˙000 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2017-COG
 Funding Scheme ERC-COG
 Starting year 2018
 Duration (year-month-day) from 2018-06-01   to  2023-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    DEUTSCHES KREBSFORSCHUNGSZENTRUM HEIDELBERG DE (HEIDELBERG) coordinator 2˙000˙000.00

Map

 Project objective

Over a million different cell types and billions of connections underlie brain function. While the embryonic brain glial progenitors generate this cellular diversity, in the adult brain progenitor competence becomes restricted to generation of few cell types. Thus, any attempt to repair the brain requires knowledge of the rules governing fate decisions within a damaged environment. We have shown that injury activates an inflammatory transcriptional signature in glial progenitors leading to exit from a dormant state. Excitingly, our recent data indicates that injury leads to demethylation of developmental enhancers in these glial progenitors too. In the regenerating zebrafish, activation of enhancers drives a transcriptional regenerative program. Yet, in rodents, despite enhancer demethylation by injury, transcription of a developmental program is missing. The overall goal of this project is to envisage ways to efficiently commission enhancers to re-direct lineage choices of glial progenitors towards re-establishing brain function following injury. Recent technological breakthroughs, including clonal lineage tracing, genome editing, and single cell “omics” combined with mouse genetics and injury models will allow (i) analysis of fate choices in the naïve and injured CNS (ii) study of how the chromatin landscape impacts transcriptional modulation of cell identity (iii) to finally design an integrated manipulation of the epigenome, transcriptome and environment for directed brain repair by endogenous progenitors. We follow a multidisciplinary approach combining cutting edge technology in functional genomics, developmental biology and translational research and leverage on a set of cutting-edge experimental platforms established in my lab and validated protocols that have led to exciting preliminary discoveries. We will provide fundamental knowledge on the mechanisms underlying lineage-decisions of CNS progenitors and open new research lines for treating CNS disorder.

 Publications

year authors and title journal last update
List of publications.
2019 Gülce S. Gülcüler Balta, Cornelia Monzel, Susanne Kleber, Joel Beaudouin, Emre Balta, Thomas Kaindl, Si Chen, Liang Gao, Meinolf Thiemann, Christian R. Wirtz, Yvonne Samstag, Motomu Tanaka, Ana Martin-Villalba
3D Cellular Architecture Modulates Tyrosine Kinase Activity, Thereby Switching CD95-Mediated Apoptosis to Survival
published pages: 2295-2306.e6, ISSN: 2211-1247, DOI: 10.1016/j.celrep.2019.10.054
Cell Reports 29/8 2020-02-06
2019 Avni Baser, Maxim Skabkin, Susanne Kleber, Yonglong Dang, Gülce S. Gülcüler Balta, Georgios Kalamakis, Manuel Göpferich, Damian Carvajal Ibañez, Roman Schefzik, Alejandro Santos Lopez, Enric Llorens Bobadilla, Carsten Schultz, Bernd Fischer, Ana Martin-Villalba
Onset of differentiation is post-transcriptionally controlled in adult neural stem cells
published pages: 100-104, ISSN: 0028-0836, DOI: 10.1038/s41586-019-0888-x
Nature 566/7742 2020-02-06
2019 Georgios Kalamakis, Daniel Brüne, Srikanth Ravichandran, Jan Bolz, Wenqiang Fan, Frederik Ziebell, Thomas Stiehl, Francisco Catalá-Martinez, Janina Kupke, Sheng Zhao, Enric Llorens-Bobadilla, Katharina Bauer, Stefanie Limpert, Birgit Berger, Urs Christen, Peter Schmezer, Jan Philipp Mallm, Benedikt Berninger, Simon Anders, Antonio del Sol, Anna Marciniak-Czochra, Ana Martin-Villalba
Quiescence Modulates Stem Cell Maintenance and Regenerative Capacity in the Aging Brain
published pages: 1407-1419.e14, ISSN: 0092-8674, DOI: 10.1016/j.cell.2019.01.040
Cell 176/6 2020-02-06

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