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CFED

Unravelling the mechanisms regulating cellular fitness during embryonic development

Total Cost €

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EC-Contrib. €

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Partnership

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Project "CFED" data sheet

The following table provides information about the project.

Coordinator
IMPERIAL COLLEGE OF SCIENCE TECHNOLOGY AND MEDICINE 

Organization address
address: SOUTH KENSINGTON CAMPUS EXHIBITION ROAD
city: LONDON
postcode: SW7 2AZ
website: http://www.imperial.ac.uk/

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 United Kingdom [UK]
 Project website https://www.imperial.ac.uk/people/tristan.rodriguez
 Total cost 183˙454 €
 EC max contribution 183˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2015
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2017
 Duration (year-month-day) from 2017-01-01   to  2018-12-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    IMPERIAL COLLEGE OF SCIENCE TECHNOLOGY AND MEDICINE UK (LONDON) coordinator 183˙454.00

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 Project objective

Understanding the mechanisms that eliminate unfit cells during development is key not only for proper organ formation but also to prevent tissue degeneration in the adult. Cell competition is a fitness quality control mechanism that occurs between cells of differing fitness levels and results in the selective elimination of those cells that, although viable, are deemed to be less fit than their neighbours. Cell competition is conserved from Drosophila to mammals and although some important regulators of this process have been identified, the mechanisms by which less-fit cells are eliminated are not well understood. Preliminary work in the Rodriguez laboratory has identified the mTOR pathway, a key metabolic sensor, as a possible regulator of cell competition in pluripotent stem cells. A small molecule screen for modulators of cell competition identified that inhibiting mTOR enhances defective pluripotent stem cell elimination during competition, and further studies revealed that mTOR activity is decreased in loser cells when confronted with winner cells. I will study the possibility that mTOR acts as a sensor of the competitive nature of pluripotent stem cells. The specific aims of this project are to find what pathways lead to differential mTOR activation during competition and unravel the mechanisms by which loss of mTOR leads to the elimination of defective stem cells. To answer these questions I will use mouse embryonic stem cells, as well as validate the in vivo relevance of my findings by studying the mouse embryo.

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