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MADMpancreas SIGNED

Using the precision mouse genetic tool MADM to elucidate the role of EGFR in directing beta cell differentiation and pancreatic morphogenesis

Total Cost €

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EC-Contrib. €

0

Partnership

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 MADMpancreas project word cloud

Explore the words cloud of the MADMpancreas project. It provides you a very rough idea of what is the project "MADMpancreas" about.

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Project "MADMpancreas" data sheet

The following table provides information about the project.

Coordinator
KOBENHAVNS UNIVERSITET 

Organization address
address: NORREGADE 10
city: KOBENHAVN
postcode: 1165
website: www.ku.dk

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 Denmark [DK]
 Total cost 207˙312 €
 EC max contribution 207˙312 € (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-ST
 Starting year 2019
 Duration (year-month-day) from 2019-06-01   to  2021-05-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KOBENHAVNS UNIVERSITET DK (KOBENHAVN) coordinator 207˙312.00

Map

 Project objective

Insulin producing beta cells are derived from bipotent pancreatic progenitors (bi-PPs) that constitute the primitive ductal epithelium. While we now know a great deal about the transcriptional networks required for endocrinogenesis and commitment to the beta lineage, considerably less is understood about the cellular events that initiate delamination and activate differentiation networks. The host group recently found that ligand-specific Egfr signaling is essential for these processes. Signaling by the highly potent Egfr ligand betacellulin diminishes apicobasal polarity leading to upregulation of Ngn3, delamination, and beta cell differentiation. The overall aim of this proposal is to elucidate the role of Egfr signaling in the beta cell differentiation process. I will ask: Is the seemingly stochastic differentiation of bi-PPs regulated by inherent differential Egfr signaling? Do quantitative differences in this single pathway lead to different cellular outcomes? How does the targeted loss of Egfr in Ngn3-expressing endocrine precursors affect their differentiation? What are the genes regulated by Egfr pathway activation that putatively commit Ngn3 progenitors to a beta cell fate? And how does the disruption of endocrine differentiation affect ductal morphogenesis? Answers to these questions have remained elusive because of the difficulty of observing individual cell behaviors in situ in the developing pancreas. To meet this challenge, I will adapt the cutting edge mouse genetic tool Mosaic Analysis with Double Markers (MADM) to quantitatively manipulate Egfr levels in bi-PPs and to concomitantly label altered cells. The successful implementation of MADMouse will deliver findings of immediate interest to investigators seeking to improve the directed differentiation of therapeutic grade beta cells from hPSCs. I will augment my expertise in precision mouse genetics with training in hESC culture enhancing my career goal of establishing my own research group.

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

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