DAMAGE BYPASS

Mechanistic analysis of DNA damage bypass in the context of chromatin and genome replication

Coordinatore	INSTITUT FUR MOLEKULARE BIOLOGIE GGMBH    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Germany [DE]
Totale costo	2˙476˙388 €
EC contributo	2˙476˙388 €
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)	2013-03-01   -   2018-02-28

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	INSTITUT FUR MOLEKULARE BIOLOGIE GGMBH  Organization address address: ACKERMANNWEG 4 city: MAINZ postcode: 55128 contact info Titolo: Ms. Nome: Franziska Cognome: Hornig Email: send email Telefono: 4961310000000 Fax: +49 6131 39 21421	DE (MAINZ)	hostInstitution	2˙476˙388.50
2	INSTITUT FUR MOLEKULARE BIOLOGIE GGMBH  Organization address address: ACKERMANNWEG 4 city: MAINZ postcode: 55128 contact info Titolo: Prof. Nome: Helle Doerte Cognome: Ulrich Email: send email Telefono: +49 6131 39 21490 Fax: +49 6131 39 21421	DE (MAINZ)	hostInstitution	2˙476˙388.50

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 Obiettivo del progetto (Objective)

'During its duplication, DNA, the carrier of our genetic information, is particularly vulnerable to decay, and the capacity of cells to deal with replication stress has been recognised as a major factor protecting us from genome instability and cancer. A major pathway that allows cells to overcome or bypass DNA lesions during replication is activated by posttranslational modifications of the sliding clamp protein PCNA. Whereas monoubiquitylation of PCNA allows mutagenic translesion synthesis by damage-tolerant DNA polymerases, polyubiquitylation is required for an error-free pathway that involves template switching to the undamaged sister chromatid, involving a recombination-like mechanism. Hence, damage bypass contributes to genome maintenance, but can itself be a source of genomic instability. It is therefore not surprising that PRR is a highly regulated process whose activity is limited to the appropriate situations by stringent control mechanisms. The proposed project aims at understanding DNA damage bypass in its cellular context. Using a combination of new and established technology, we will address the role of chromatin dynamics in the reaction, its spatial and temporal control in relation to genome replication, and its coordination with other PCNA-dependent processes in the cell. To this end, we will establish technology to isolate and analyse the composition of damage bypass tracts, develop and implement novel methods to induce lesions and image damage processing in live cells, and exploit a spectrum of biochemical and biophysical techniques to investigate the role of PCNA as a molecular tool-belt in the coordination of its interaction partners. In combination, these approaches will give important insight into how the replication of damaged DNA is managed with high efficiency and accuracy within the cell.'