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Nucleolar Responses to DNA Damage: rDNA, an emerging hub of genome instability

Total Cost €


EC-Contrib. €






 NUCDDR project word cloud

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

organization    source    links    nucleolus    pertinent    constitute    malignant    caused    signaling    explore    regulating    repetitive    environment    integrity    yield    impose    experimental    corrupted    damage    viability    regulators    therapeutic    biology    loci    display    threats    genomic    enrichment    histone    rna    diagnostic    heavily    instability    expression    human    lesions    oncogene    networks    molecular    nucleolar    rearrangements    membrane    hybrids    rdna    chromatin    neoplastic    suppressors    imaging    chromosomes    susceptibility    certain    sequences    clusters    applicable    primary    cell    gene    hypothesis    tumour    hallmarks    strategies    dna    transcribed    models    whereas    live    insights    genome    repair    anywhere    mass    malignancy    biological    tools    transformation    inactivation    serious    replication    spectrometry    recapitulate    nuclear    transcription    area    uncover    linked    epigenetic    stress    ribosomal    rigorously    cancer    inducible    chromosomal    mechanisms    putative    hub    organelle   

Project "NUCDDR" data sheet

The following table provides information about the project.


Organization address
postcode: 265 04

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 Greece [EL]
 Total cost 1˙499˙525 €
 EC max contribution 1˙499˙525 € (100%)
 Programme 1. H2020-EU.1.1. (EXCELLENT SCIENCE - European Research Council (ERC))
 Code Call ERC-2019-STG
 Funding Scheme ERC-STG
 Starting year 2020
 Duration (year-month-day) from 2020-06-01   to  2025-05-31


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    PANEPISTIMIO PATRON EL (RIO PATRAS) coordinator 1˙499˙525.00


 Project objective

DNA lesions can impose serious threats to genome integrity and cell viability. Whereas DNA damage may occur anywhere in the genome, it is increasingly recognized that certain genomic loci rich in repetitive sequences display increased susceptibility to damage and are linked to chromosomal rearrangements and malignancy. Clusters of ribosomal DNA gene (rDNA) repeats, present on five different chromosomes, constitute the most heavily transcribed area of the human genome and are organized in a nuclear membrane-less organelle, the nucleolus. So far, putative links between rDNA damage and malignant processes have not been rigorously assessed. We will address the hypothesis that rDNA repeats represent a major hub of genomic instability contributing to malignant transformation. Using state-of-the-art experimental systems that allow enrichment for nucleolar DNA damage, we will explore: (i) hypothesis-driven and mass spectrometry-based approaches to define regulators of the rDNA damage response; (ii) live imaging and advanced molecular biology tools to uncover how histone epigenetic changes and formation of RNA:DNA hybrids impact on nucleolar chromatin, nucleolar organization, rDNA transcription and repair ; (iii) cell models that recapitulate malignant transformation caused by inducible oncogene expression or epigenetic inactivation of tumour suppressors, to assess replication stress in rDNA repeats as a primary source of genomic instability and pertinent to hallmarks of cancer. The proposed research is expected to yield novel insights into the signaling networks and biological processes regulating rDNA damage and repair within the nuclear environment and define how these mechanisms are corrupted during neoplastic transformation. This knowledge could be directly applicable to the design of new diagnostic or therapeutic strategies for cancer.

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

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