EPIMECHANISM

Mechanisms of Chromatin-based Epigenetic Inheritance

 Coordinatore FUNDACAO CALOUSTE GULBENKIAN 

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 Nazionalità Coordinatore Portugal [PT]
 Totale costo 1˙621˙400 €
 EC contributo 1˙621˙400 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call ERC-2013-CoG
 Funding Scheme ERC-CG
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-06-01   -   2019-05-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    FUNDACAO CALOUSTE GULBENKIAN

 Organization address address: AVENIDA DE BERNA 45A
city: LISBOA
postcode: 1000

contact info
Titolo: Dr.
Nome: Lars
Cognome: Jansen
Email: send email
Telefono: +35 1 214464519
Fax: +35 1 214407970

PT (LISBOA) hostInstitution 1˙621˙400.00
2    FUNDACAO CALOUSTE GULBENKIAN

 Organization address address: AVENIDA DE BERNA 45A
city: LISBOA
postcode: 1000

contact info
Titolo: Mr.
Nome: Jose Mario
Cognome: Leite
Email: send email
Telefono: +35 1 214407937
Fax: 351214000000

PT (LISBOA) hostInstitution 1˙621˙400.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

nucleosomes    strategy    cells    cenp    locus    cell    memory    determine    dna    centromere    histone    chromatin    cycle    coupling    epigenetic    local    chromosome    duplication    uncover    inherited   

 Obiettivo del progetto (Objective)

'Epigenetic mechanisms heritably maintain gene expression states and chromosome organization across cell division. These include chromatin-based factors that are propagated independent of local DNA sequence elements, and are critical for normal development and prevent reprogramming, e.g. during induction of pluripotency. We focus on the role of nucleosomes, the histone-DNA complexes that make up chromatin. While prominently implicated in epigenetic memory, how histones and their local modifications can actually be inherited is largely unknown. We take aim at three fundamental aspects that we argue are central to this problem: stability of the epigenetic mark, self-templated duplication, and cell cycle coupling. We developed a unique pulse-labeling strategy to determine whether silent and active chromatin can be inherited and how this relates to transcription, both in cancer cells and in vitro differentiating stem cells. By coupling this strategy to an imaging-based RNAi screen we aim to identify components controlling nucleosome assembly and heritability. We achieve this by focusing on the human centromere, the chromosome locus essential for chromosome segregation which serves as an ideal model for epigenetic memory. This locus is specified by nucleosomes carrying the histone H3 variant, CENP-A that we have previously shown to be highly stable in cycling cells and to be replicated in a strict cell cycle coupled manner. We build on our previous successes to uncover the molecular mechanism and cellular consequences of the coupling between CENP-A propagation and the cell cycle which we postulate, ensures proper centromere size and mitotic fidelity. Furthermore, by genome engineering we developed a strategy to delete an endogenous centromere to determine how centromeres can form de novo and how CENP-A chromatin, once formed, can template its own duplication. With this multi-facetted approach we aim to uncover general mechanistic principles of chromatin-based memory.'

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