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RecInRep SIGNED

Beyond double-strand break repair: specific mechanisms of homologous recombination at stressed replication forks.

Total Cost €

0

EC-Contrib. €

0

Partnership

0

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 RecInRep project word cloud

Explore the words cloud of the RecInRep project. It provides you a very rough idea of what is the project "RecInRep" about.

cancer    protecting    genetic    mediated    replicating    recombination    force    transient    determinants    host    molecule    gain    holistic    instrumental    vitro    shown    forks    tumourigenesis    received    modulating    techniques    highlighted    mutations    believe    biology    combines    background    microscopy    first    template    biochemically    expertise    regulators    mechanistic    conferred    genes    causative    instability    recruitment    transaction    multidisciplinary    tolerate    mechanisms    transformation    strategies    single    reversal    genomic    vivo    basis    besides    cancers    recombinase    stress    fork    mediate    central    chromosomes    strand    unknown    groundwork    break    beginning    combination    replication    driving    protection    homologous    strategy    molecular    rad51    specialized    remodelling    junctions    chemotherapeutic    dna    proteins    biochemical    catalyse    emerge    repair    damage    double    lab    caretaker    defective    regulate    assist    genotoxic    screen    hr    therapy    uncovering    interference    predisposition    cell   

Project "RecInRep" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITAT ZURICH 

Organization address
address: RAMISTRASSE 71
city: Zürich
postcode: 8006
website: http://www.unizh.ch

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country Switzerland [CH]
 Project website http://www.imcr.uzh.ch/en/research/Lopes.html
 Total cost 175˙419 €
 EC max contribution 175˙419 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2015
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2016
 Duration (year-month-day) from 2016-04-01   to  2018-03-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITAT ZURICH CH (Zürich) coordinator 175˙419.00

Map

 Project objective

Genomic instability is the main driving force of tumourigenesis, as highlighted by the cancer predisposition conferred by mutations in caretaker genes. DNA replication stress has recently received much attention, for its causative role in transformation and as a strategy for cancer therapy. Besides other mechanisms protecting replicating chromosomes from genotoxic stress, transient fork remodelling into four-way junctions (fork reversal) is emerging as a key transaction to assist template repair or to tolerate DNA damage and replication interference. Factors and mechanisms modulating this transaction are just beginning to emerge. The central recombinase RAD51 was recently shown to promote fork reversal, uncovering a fork-specific role for homologous recombination (HR) proteins, beyond their established role in the double-strand break repair. However, the molecular determinants controlling RAD51-mediated fork remodelling are yet unknown. I propose to gain mechanistic insight into the role of RAD51 and other HR proteins in replication stress, using an integrated, multidisciplinary approach, which combines my current biochemical expertise with specialized cell biology and single-molecule techniques available in the host lab. In particular, I will first set up a microscopy-based screen to identify factors that regulate RAD51 recruitment at replication forks upon stress. Then, I will use a combination of single-molecule and cell biology techniques to investigate how these novel RAD51 regulators mediate in vivo RAD51 role in fork protection and remodelling. Finally, I will establish an in vitro system to study biochemically the mechanisms by which RAD51 and the novel identified factors catalyse replication fork remodelling. I believe that this 'holistic' approach will be instrumental not only to define the molecular basis of cancers with a HR-defective genetic background, but also to provide the groundwork to develop more effective chemotherapeutic strategies.

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The information about "RECINREP" are provided by the European Opendata Portal: CORDIS opendata.

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