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    Heterochromatin dynamics in aged and cancer cells: facultative heterochromatin erosion as driver for cellular reorganization?

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    Séminaire de l'Institut Cochin

    Jeudi 21 mars 2019 - 12h00 - Salle de conférence Rosalind Franklin, 2ème étage

     

    Daan Noordermeer
    Daan Noordermeer

    Institute for Integrative Biology ot the Cell (I2BC), Gif sur Yvette

     

     invité par Pascal Maire

    Institut Cochin, 22 rue Méchain, 75014 Paris

     

    Résumé

     The correct repression of genes is crucial to maintain correct identity and function of cells. Repressed genes can be present in a dedicated chromatin environment, called heterochromatin. The heterochromatin environment can be constitutive, where repression is thought to be permanent, or facultative, where repression is reversible.
    In aged and cancer cells, a profound reorganization of heterochromatin structure and organization has been observed. Until now though, a complete understanding of these changes is lacking, mostly due to the use of different experimental models and a lack of systematic integration.
    We have combined imaging, RNA-seq, ChIP-seq and Hi-C to systematically characterize the dynamics of heterochromatin structure in in-vivo aged mouse cells and in the WEHI-231 cellular model for B-cell lymphoma. We find that during aging, particularly the facultative heterochromatin domain becomes less defined and structured. This erosion is accompanied by a less stable repression of genes in this domain. Loss of facultative heterochromatin is mildly compensated by the H3K9me2 histone mark, which is normally associated with constitutive heterochromatin. During aging, the erosion of heterochromatin structure and function therefore appears most prominent in the facultative domain.
    In B-cell lymphoma, we find a considerably more profound erosion of both the facultative and constitutive heterochromatin domains. This global reorganization is accompanied by a strong derepression of genes in both domains. Heterochromatin reorganization in cancer cells can therefore be considerably more drastic, with both shared and differential characteristics as compared to aging.

     

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