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

Project description

Specific genomic areas as hotspots for cancer transformation

DNA is a macromolecule that contains our genetic information, constantly found under attack resulting in DNA damage. Failure to repair this damage is associated with numerous diseases, cancer being the most prominent one. Certain DNA features including sequence repetition and spatial organisation can make DNA more susceptible to damage or more difficult to repair. The ribosomal DNA (rDNA) is mostly known for coding ribosomal RNA, a molecule critical to protein synthesis. Special characteristics of rDNA, including high rates of rRNA generation, repetitive nature and spreading into different chromosomes, may constitute rDNA repeats a hotspot of cancer transformation. The EU-funded NUCDDR project is exploiting this hypothesis, investigating rDNA damage, repair mechanisms and the potential correlation between rDNA damage and cancer.

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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ERC-STG - Starting Grant

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(opens in new window) ERC-2019-STG

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Host institution

PANEPISTIMIO PATRON
Net EU contribution

Net EU financial contribution. The sum of money that the participant receives, deducted by the EU contribution to its linked third party. It considers the distribution of the EU financial contribution between direct beneficiaries of the project and other types of participants, like third-party participants.

€ 1 499 525,00
Address
UNIVERSITY CAMPUS RIO PATRAS
265 04 RIO PATRAS
Greece

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Region
Κεντρική Ελλάδα Δυτική Ελλάδα Αχαΐα
Activity type
Higher or Secondary Education Establishments
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Total cost

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€ 1 499 525,00

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