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SUMiDENTITY SIGNED

Deconstructing the role of SUMO on chromatin in cell identity and tissue repair

Total Cost €

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EC-Contrib. €

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Partnership

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 SUMiDENTITY project word cloud

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

roles    mechanisms    underlying    desumoylation    toward    accompanies    uncovered    stabilizer    fate    dynamics    disease    barrier    substrates    complexes    locus    determined    dynamic    repair    provides    notably    reciprocally    maintaining    conjugating    poorly    loci    critical    resisting    deconjugating    avenues    acts    specify    muscle    complementary    plays    determinants    cell    cellular    tissue    subverted    mechanism    escs    central    configurations    fibroblasts    questions    pluripotent    chromosomal    paradigm    molecular    experimental    medicine    interplay    injury    deposits    existence    biology    opening    regulators    bound    reprogramming    effort    transitions    transcription    druggable    pathophysiological    pluripotency    treatment    paradigmatic    balance    somatic    regenerative    chromatin    function    actively    integrate    principally    equilibrium    specifications    gene    explore    cancer    mark    maintenance    functions    safeguard    vision    sumo    enforces    transition    identity    rapid    corrupted    transcriptional    sumoylation    regulated    regulatory    totipotent    identities    types    distinctive    regulating   

Project "SUMiDENTITY" data sheet

The following table provides information about the project.

Coordinator
INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE 

Organization address
address: RUE DE TOLBIAC 101
city: PARIS
postcode: 75654
website: www.inserm.fr

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 France [FR]
 Total cost 2˙499˙995 €
 EC max contribution 2˙499˙995 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-ADG
 Funding Scheme ERC-ADG
 Starting year 2020
 Duration (year-month-day) from 2020-01-01   to  2024-12-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE FR (PARIS) coordinator 2˙499˙995.00

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 Project objective

The maintenance of cell identity and how it is subverted in disease are central questions in biology and medicine. The interplay between transcription factor and chromatin configurations plays a key role in maintaining cellular identity, yet how this interplay is regulated is poorly understood. Notably, the existence of possible general mechanisms underlying different cell-state specifications remains to be determined. We have recently uncovered evidence that sumoylation, which deposits a chromatin-associated mark (SUMO) that principally targets transcriptional regulators, acts as a general barrier to cell-fate transitions and enforces two distinctive chromatin types to safeguard somatic and pluripotent cell identities. The central paradigm for the proposed work is that SUMO functions as a general stabilizer of critical chromatin-bound determinants of cell identity and that the equilibrium between conjugating/deconjugating activities provides a general regulatory mechanism for their dynamic targeting to key chromosomal loci, thus actively contributing to cell-fate change. Focusing on reprogramming to pluripotency and transition to totipotent-like states, we propose to: 1) identify relevant locus-specific SUMO substrates/complexes in fibroblasts and ESCs, 2) define the role of SUMO in regulating their function and dynamics and, reciprocally, 3) explore the sumoylation/desumoylation balance that accompanies cell-fate change. A complementary effort seeks 4) to exploit these experimental approaches to study a paradigmatic pathophysiological process involving rapid cell-fate transitions: tissue repair following muscle injury. With a vision toward targeting this druggable pathway for regenerative medicine and cancer treatment, we expect these studies to integrate the gene regulatory roles of SUMO in resisting cell-fate change, thus opening up new avenues to the molecular mechanisms that specify cell identity during development and to how they are corrupted in disease.

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