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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.

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

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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