VRNEPIGEN
Maintenance of cellular memory by the Arabidopsis VRN1 protein
| Coordinatore | JOHN INNES CENTRE
Organization address
address: "Norwich Research Park, Colney" contact info |
| Nazionalità Coordinatore | United Kingdom [UK] |
| Totale costo | 0 € |
| EC contributo | 179˙649 € |
| 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-IEF-2008 |
| Funding Scheme | MC-IEF |
| Anno di inizio | 2009 |
| Periodo (anno-mese-giorno) | 2009-03-01 - 2011-02-28 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 |
JOHN INNES CENTRE
Organization address
address: "Norwich Research Park, Colney" contact info |
UK (NORWICH) | coordinator | 179˙649.73 |
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Obiettivo del progetto (Objective)
'Modifications of a cells chromatin landscape enable cells to memorize and maintain gene expression profiles throughout many cell-cycles during development. In animals and plants the Polycomb Repressive Complex 2 (PRC2) is involved in maintaining genes in an epigenetic “off” state. In mammals and flies a second complex, PRC1, collaborates with PRC2 to maintain silencing. Interestingly, other organisms including worms and plants lack PRC1 and it remains elusive how they achieve stable silencing. In Arabidopsis the DNA-binding protein VRN1 is a potential candidate to fulfil such a role in silencing. During a cold-induced process called vernalization, the floral repressor gene FLC is epigenetically repressed and maintained inactive by a plant PRC2 and VRN1. Lack of VRN1 does not impair PRC2 function but seems to act downstream or in parallel of PRC2, a situation analogous to animal PRC1. Moreover, as found for mammalian PRC1, VRN1 interacts with a component of the spliceosome complex, implying RNA processing in Polycomb silencing. The above findings suggest that VRN1, despite its lack of homology with PRC1 components, functions in the stable maintenance of PRC2 mediated silencing. My aim is to establish a solid foundation for a mechanistic understanding of VRN1 mediated gene silencing using vernalization as a model. In-depth VRN1 protein-complex analysis will be complemented by chromatin and RNA immuno-precipitations (ChIP and RIP) as well as theoretical modelling of the vernalization process. Besides addressing a long-standing question in plant epigenetics, collected data will allow comparison with the situation in non-plant systems to develop a mechanistic consensus model on maintenance of gene silencing in different kingdoms. Notably, for both plants and humans, fundamental knowledge of epigenetics will facilitate the modulation of gene expression to; increase yield and disease resistance in crops and develop treatments for diseases, such as cancer, in humans.'