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Centromere Stability SIGNED

Mechanisms that maintain centromere DNA repeats stability in human cells.

Total Cost €

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EC-Contrib. €

0

Partnership

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 Centromere Stability project word cloud

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

lines    preventing    connect    poorly    molecular    sister    constitutive    network    foundation    cancers    aid    stability    rearrangements    pcr    division    conceptual    aging    arrays    array    impeding    maintained    spindle    throughput    mechanisms    variety    ideated    sequence    chromosomes    ccan    editing    maintenance    defects    replication    shortening    fragility    chromosome    circumvent    framework    play    cas    imaging    examine    human    ploidy    aberrant    inducible    fish    repetitive    cancer    independent    barriers    giunta    prevent    incomplete    proliferation    mitosis    cell    cen    cenp    genome    driving    fellowship    stable    age    qrt    lay    chromatids    degron    instability    subsequent    unveil    situ    qfish    chromosomal    centromere    funabiki    dysfunction    revealed    assays    auxin    data    separating    2018    2017    cytogenetic    senescence    technique    co    dynamics    size    relies    fluorescence    crispr    dna    damage    hybridization    cells    disease    aneuploidy    innovative    sites    annotation    altogether    centromeres    primary    orientation    compromised    validated    undergoing    physiology    proteins   

Project "Centromere Stability" data sheet

The following table provides information about the project.

Coordinator
UNIVERSITA DEGLI STUDI DI ROMA LA SAPIENZA 

Organization address
address: Piazzale Aldo Moro 5
city: ROMA
postcode: 185
website: www.uniroma1.it

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 Italy [IT]
 Total cost 183˙473 €
 EC max contribution 183˙473 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2018
 Funding Scheme MSCA-IF-EF-RI
 Starting year 2020
 Duration (year-month-day) from 2020-09-01   to  2022-08-31

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    UNIVERSITA DEGLI STUDI DI ROMA LA SAPIENZA IT (ROMA) coordinator 183˙473.00

Map

 Project objective

Cell division relies on centromeres, which connect chromosomes to the spindle for separating sister chromatids in mitosis. Human centromeres are composed of large arrays of repetitive DNA, which are often sites of aberrant rearrangements in cancer. While centromere defects can cause chromosomal instability, the molecular mechanisms that maintain their repetitive DNA stable are poorly understood. During the fellowship, I aim to investigate how human centromere stability is maintained and the consequences of centromere dysfunction in driving cancer and aging. To circumvent impeding technical barriers due to incomplete centromere sequence annotation, I have ideated the use of Chromosome Orientation Fluorescence In Situ Hybridization at human centromeres (Cen-CO-FISH; Giunta, 2018). Using this innovative technique, I revealed that CENP-A and CCAN (constitutive centromere-associated network) proteins prevent centromere instability, and this functionality is compromised in cancer cell lines and in primary cells undergoing senescence (Giunta & Funabiki, 2017); my data show that CENP-A may play a new role during centromere replication, preventing DNA damage, repeats shortening, and subsequent aneuploidy. I will use the Auxin-Inducible Degron (AID) system and CRISPR-Cas genome editing with high-throughput imaging of Cen-CO-FISH to identify the human centromere maintenance network and investigate the mechanisms of repeats stability. I will also examine the consequences of centromeres dysfunction, including changes in the size of the array, cell ploidy and proliferation dynamics, using a variety of validated and novel methods, including Cen-qRT-PCR, qFISH and cytogenetic assays. Altogether, the proposed research will unveil a novel conceptual framework to explain the fragility of repetitive centromere DNA and its consequences on cell physiology and disease. This work will lay the foundation for my future independent research on centromere instability in age-associated cancers.

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