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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.

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

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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