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Accueil > Séminaires

Département Biologie des Génomes

par EQYY - publié le , mis à jour le

Agenda

  • Vendredi 15 décembre 11:00-12:00 - Wouter de Laat - Biomedical genomics group, Hubrecht Institute, Utrecht, The Netherlands

    Genome structure-function relationships explored at new dimensions

    Résumé : Chromatin folding is increasingly recognized as a regulator of genomic processes such as gene activity. Chromosome conformation capture (3C) methods have been developed to unravel genome topology through the analysis of pair-wise chromatin contacts and have identified many genes and regulatory sequences that, in populations of cells, are engaged in multiple DNA interactions. I will describe our contributions to this field and will present novel Multi-Contact 4C (MC-4C), that applies Oxford Nanopore long-read single molecule sequencing to study multi-way DNA conformations of individual alleles for distinction between cooperative, random and competing interactions. Using this single molecule multi-contact analysis method, we uncover previously missed structures in sub-populations of cells, reveal single locus enhancer hubs and demonstrate the collision of CTCF-anchored architectural loops. Insight into single allele higher-order topological features will help understanding how the myriad of regulatory sequences spatially coordinate their actions on individual chromosomes and facilitate interpreting the consequences of natural and induced genetic variation. If time permits, I will also discuss how we explore the application of 3C-based methods in DNA diagnostics, oncogenetics and non-invasive prenatal diagnosis.
    Contact : Daan Noordermeer <daan.noordermeer i2bc.paris-saclay.fr>

    Lieu : Auditorium - bâtiment 21 - Campus CNRS de Gif-sur-Yvette


  • Lundi 15 janvier 2018 14:00-15:00 - Annabelle Decottignies - de Duve Institute, Brussels

    Revisiting cellular immortality in melanoma

    Résumé : Unlimited replicative potential is one of the hallmarks of cancer cells. In melanoma, hTERT (telomerase reverse transcriptase) is frequently overexpressed because of activating mutations in its promoter, suggesting that telomerase is necessary for melanoma development. We observed, however, that a subset of melanoma metastases and derived cell lines had no telomere maintenance mechanism. Early passages of the latter displayed long telomeres that progressively shortened and fused before cell death. We propose that, during melanoma formation, oncogenic mutations occur in precursor melanocytes with long telomeres, providing cells with sufficient replicative potential, thereby bypassing the need to re-activate telomerase. Our data further support the emerging idea that long telomeres promote melanoma formation. These observations are important when considering anticancer therapies targeting telomerase.
    Contact : Laure CRABBE <Laure.CRABBE i2bc.paris-saclay.fr>

    Lieu : Auditorium - bâtiment 21 - Campus CNRS de Gif-sur-Yvette


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