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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.

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

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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