Explore the words cloud of the SUMiDENTITY project. It provides you a very rough idea of what is the project "SUMiDENTITY" about.
The following table provides information about the project.
INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE
|Coordinator Country||France [FR]|
|Total cost||2˙499˙995 €|
|EC max contribution||2˙499˙995 € (100%)|
1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
|Duration (year-month-day)||from 2020-01-01 to 2024-12-31|
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|1||INSTITUT NATIONAL DE LA SANTE ET DE LA RECHERCHE MEDICALE||FR (PARIS)||coordinator||2˙499˙995.00|
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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