SSB REPAIR

Molecular analysis of single-strand break repair (SSBR) in human cells

Coordinatore	UNIVERSITY OF SUSSEX    more  Organization address address: Sussex House city: FALMER, BRIGHTON postcode: BN1 9RH contact info Titolo: Mr. Nome: Peter Graham Cognome: Brooks Email: send email Telefono: 00 44 1273 877718 Fax: 00 44 1273 678192
Nazionalità Coordinatore	United Kingdom [UK]
Totale costo	178˙307 €
EC contributo	178˙307 €
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-2007-2-1-IEF
Funding Scheme	MC-IEF
Anno di inizio	2008
Periodo (anno-mese-giorno)	2008-07-01   -   2010-06-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	UNIVERSITY OF SUSSEX  Organization address address: Sussex House city: FALMER, BRIGHTON postcode: BN1 9RH contact info Titolo: Mr. Nome: Peter Graham Cognome: Brooks Email: send email Telefono: 00 44 1273 877718 Fax: 00 44 1273 678192	UK (FALMER, BRIGHTON)	coordinator	0.00

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 Obiettivo del progetto (Objective)

'DNA single-strand breaks (SSBs) can arise directly by the action of free radicalsor indirectly as intermediates of base excision repair or topoisomerase I activity. Moreover, replication can convert a SSB into a double-strand break (DSB), one of the most severe DNA lesions that can occur in living cells. Single-strand break repair (SSBR) is therefore crucial to ensure cell survival and the maintenance of genome stability. In addition, SSBR defects have been associated with some neurodegenerative diseases.The main goal of this project is to study the molecular mechanism/s of SSBR in human cells. Our primary focus will be to develop a novel system to induce a site-specific SSB in human cells. This will allow, for the first time, direct analysis of the assembly/disassembly of protein complexes at the SSB reaction by ChIP analyses, in addition to measuring the repair event itself. For example, we will examine the sequence of recruitment of the individual SSBR proteins, as well as identifying which proteins are required for assembly/disassembly/remodelling of protein complexes at chromosomal SSBs. This approach will also provide a system to examine possible SSBR defects in neurodegenerative diseases. We are particullary interested in defining the molecular role of APLF (aprataxin and PNK like factor), a SSBR protein recently identified in this laboratory.'