REPROGRAMMING

Molecular mechanisms leading to genome-wide DNA demethylation during epigenetic reprogramming

Coordinatore	IMPERIAL COLLEGE OF SCIENCE, TECHNOLOGY AND MEDICINE    more  Organization address address: SOUTH KENSINGTON CAMPUS EXHIBITION ROAD city: LONDON postcode: SW7 2AZ contact info Titolo: Ms. Nome: Tatjana Cognome: Palalic Email: send email Telefono: 442076000000 Fax: 442076000000
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	199˙549 €
EC contributo	199˙549 €
Programma	FP7-PEOPLE Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
Code Call	FP7-PEOPLE-2010-IEF
Funding Scheme	MC-IEF
Anno di inizio	2011
Periodo (anno-mese-giorno)	2011-04-01   -   2013-03-31

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	IMPERIAL COLLEGE OF SCIENCE, TECHNOLOGY AND MEDICINE  Organization address address: SOUTH KENSINGTON CAMPUS EXHIBITION ROAD city: LONDON postcode: SW7 2AZ contact info Titolo: Ms. Nome: Tatjana Cognome: Palalic Email: send email Telefono: 442076000000 Fax: 442076000000	UK (LONDON)	coordinator	199˙549.60

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 Obiettivo del progetto (Objective)

'Epigenetic reprogramming is a developmental process involving both genome-wide DNA demethylation and chromatin remodelling. Under physiological conditions it occurs at distinct stages of normal embryonic development. However, under in vitro conditions induction of this process can restore pluripotency in somatic cells, and in aberrant situations a similar dedifferentiation process can initiate carcinogenesis. While the kinetics of the reprogramming that occurs in the course of normal development has been well documented, initial steps inducing this process and how DNA methylation marks are removed in vivo remain elusive. The involvement of DNA repair mechanisms in DNA demethylation during epigenetic reprogramming has been recently suggested. The presented project proposes to investigate the upstream events initiating epigenetic reprogramming by using both in vivo and in vitro approaches. We will focus on recently discovered candidates involved in 5-methylcytosine hydroxylation and will investigate a possible involvement of this modification of 5-methylcytosine in the epigenetic reprogramming during mouse development. We will also examine the potential repair enzymes able to remove this epigenetic mark in order to highlight other protein partners involved in this process. Data obtained on this pathway will not only enrich our understanding towards developmental reprogramming, but also enhance our ability to manipulate cell fate in vitro.'