REPBLOCK
SITE-SPECIFIC DNA REPLICATION PERTURBATION AND ITS EFFECTS ON CHROMOSOME SEGREGATION
| Coordinatore | KOBENHAVNS UNIVERSITET
Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie. |
| Nazionalità Coordinatore | Denmark [DK] |
| Totale costo | 2˙456˙760 € |
| EC contributo | 2˙456˙760 € |
| 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-2012-ADG_20120314 |
| Funding Scheme | ERC-AG |
| Anno di inizio | 2013 |
| Periodo (anno-mese-giorno) | 2013-06-01 - 2018-05-31 |
Partecipanti
| # | ||||
|---|---|---|---|---|
| 1 | KOBENHAVNS UNIVERSITET | DK | hostInstitution | 2˙456˙760.00 |
| 2 | KOBENHAVNS UNIVERSITET | DK | hostInstitution | 2˙456˙760.00 |
Mappa
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Obiettivo del progetto (Objective)
'Challenges to the stable maintenance of the human genome can come from both endogenous and exogenous sources. However, one of the major threats to genome stability occurs during normal DNA metabolism. The genome is particularly susceptible to perturbation during the S-phase of the cell cycle when DNA replication occurs. This is because DNA replication forks can encounter chemical adducts, DNA secondary structures, topological constraints or bound proteins that hinder their progression. In actively proliferating cells, such as stem cells, replication perturbation can lead to fork stalling, breakage or collapse. These scenarios can, in turn, generate deleterious chromosomal rearrangements that have the potential to initiate human disease. Despite recent advances in our understanding of the biochemical process of DNA replication, the precise details of the events occurring at sites where replication forks have been perturbed remain poorly characterised. This is because in-depth analysis of the perturbation of replication represents a major technical challenge, principally because adducts and lesions generated by DNA damaging agents are randomly distributed throughout the genome at sites that cannot be controlled or predicted. To overcome this technical limitation, we have developed systems for site-specific perturbation of DNA replication that can be transferred to any locus in any cell type. The aim is to define how replication fork perturbation is detected and engaged by cellular stress-response factors, and then tolerated or repaired. This highly integrated proposal, and the pioneering technologies that will be used to fulfil our ambitious aims, will have significant implications for the understanding not only of replication perturbation and its effects on chromosome dynamics in mitosis, but also of the role of replication stress in the aetiology of cancer and premature ageing. It will open up new horizons both in and across these fields of research.'