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OCTOBER SIGNED

Control of cell identity in pluripotent and germline cells by OCT4 orchestration of chromatin binding and enhancer regulation

Total Cost €

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EC-Contrib. €

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Partnership

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Project "OCTOBER" data sheet

The following table provides information about the project.

Coordinator
THE UNIVERSITY OF EDINBURGH 

Organization address
address: OLD COLLEGE, SOUTH BRIDGE
city: EDINBURGH
postcode: EH8 9YL
website: www.ed.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]
 Total cost 212˙933 €
 EC max contribution 212˙933 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-RI
 Starting year 2019
 Duration (year-month-day) from 2019-10-28   to  2021-10-27

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    THE UNIVERSITY OF EDINBURGH UK (EDINBURGH) coordinator 212˙933.00

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 Project objective

The development of an organism requires the fine-tuned balance between self-renewal and differentiation of pluripotent cells. Pluripotency is controlled by a group of transcription factors (TFs) that constitute the Pluripotency Gene Regulatory Network (PGRN). OCT4 is a core component of the PGRN and is required to specify pluripotency in vivo and to maintain pluripotency in vitro in embryonic stem cells (ESCs). OCT4 is also required for survival of unipotent primordial germ cells (PGCs). However, it is still not clear how a pluripotency-associated TF like OCT4 can also be required in both ESCs and in more differentiated cells. In this proposal, I will address the hypothesis that OCT4 function in ESCs and PGCs requires the targeting of distinct cis-regulatory elements (CREs - enhancers and promoters) in the two systems. By comparing the genome-wide distribution of OCT4 in ESCs and PGCs, I will identify the OCT4-bound CREs specific for each cell type. Using bioinformatic tools, I will identify genes associated with these elements that distinguish between the transcriptional networks regulated by OCT4 in each cell type. In ESCs a decrease of OCT4 expression correlates with an increase in OCT4 binding to chromatin. To unveil the mechanisms underpinning this phenotype, I will perturb the OCT4 concentration in ESCs by combining targeted genome editing and protein degradation assays. I will extend studies of altering OCT4 concentration to PGCs using similar approaches. In addition, I will assess the hypothesis that physical interactions between CREs play a defining role in cell-specific gene expression. I will use 3D genome assays to determine whether the context-dependent function of OCT4 in ESCs and PGCs depends upon the regulation of distinct interactions between different sets of CREs in each cell type. Using cutting-edge assays, this action will shed light on the dual activity of OCT4 in ESCs and PGCs, providing new insights into stem cell biology.

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

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