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SafeFate SIGNED

Safeguarding Cell Fate by Terminal Repression during Development and Disease

Total Cost €

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EC-Contrib. €

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Partnership

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Project "SafeFate" 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 1˙761˙489 €
 EC max contribution 1˙761˙489 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2018-STG
 Funding Scheme ERC-STG
 Starting year 2019
 Duration (year-month-day) from 2019-02-01   to  2024-01-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    DEUTSCHES KREBSFORSCHUNGSZENTRUM HEIDELBERG DE (HEIDELBERG) coordinator 1˙761˙489.00

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 Project objective

Cell identity and function requires both induction of desired genes and repression of unwanted programs. While master regulators that activate gene networks during development are well characterized, the mechanisms that terminally repress alternative fates remain poorly understood. Within this project, I aim to demonstrate that active terminal repression is a universal mechanism required to prevent loss of cell identity and disease.

We recently found that the neuron-specific transcription repressor Myt1l is essential to induce neuronal cell identity. Myt1l is expressed in virtually all neurons throughout life and its loss in mature neurons impairs neuronal gene expression and function, suggesting a role in maintaining cell fate. Unlike known repressors such as REST that specifically silences neuronal genes in non-neuronal cells, Myt1l represses many non-neuronal programs in neurons. I therefore propose that a new class of terminal repressor exists that continuously represses alternative lineages to confer and maintain cell identity.

Since Myt1l mutations often occur in autism and schizophrenia I will investigate how loss of terminal repression can contribute to these poorly understood but common mental disorders. This will require molecular and behavioural studies in human and mouse models. We will also investigate how a sequence specific terminal repressor biochemically interacts with general epigenetic machinery to continuously silence unwanted programs during neuronal reprogramming. Finally, we will test candidate terminal repressors in other lineages by loss and gain of function approaches to analyse whether terminal repression is a universal principle of biology. Ultimately this will provide insight into fighting diseases associated with loss of cell identity and to efficiently generate cells for regenerative medicine using reprogramming.

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The information about "SAFEFATE" are provided by the European Opendata Portal: CORDIS opendata.

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