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Marking of active genes on mitotic chromosomes

Author

Listed:
  • Emil F. Michelotti

    (Gene Regulation Section, Laboratory of Pathology, National Cancer Institute, National Institutes of Health)

  • Suzanne Sanford

    (Gene Regulation Section, Laboratory of Pathology, National Cancer Institute, National Institutes of Health)

  • David Levens

    (Gene Regulation Section, Laboratory of Pathology, National Cancer Institute, National Institutes of Health)

Abstract

During development and differentiation, cellular phenotypes are stably propagated through numerous cell divisions1. This epigenetic ‘cell memory’ helps to maintain stable patterns of gene expression2. DNA methylation3 and the propagation of specific chromatin structures may both contribute to cell memory4. There are two impediments during the cell cycle that can hinder the inheritance of specific chromatin configurations: first, the pertinent structures must endure the passage of DNA-replication forks in S phase5; second, the chromatin state must survive mitosis, when chromatin condenses, transcription is turned off, and almost all double-stranded DNA-binding proteins are displaced6,7. After mitosis, the previous pattern of expressed and silent genes must be restored. This restoration might be governed by mass action, determined by the binding affinities and concentrations of individual components. Alternatively, a subset of factors might remain bound to mitotic chromosomes, providing a molecular bookmark to direct proper chromatin reassembly. Here we analyse DNA at transcription start sites during mitosis invivo and find that it is conformationally distorted in genes scheduled forreactivation but is undistorted in repressed genes. Theseprotein-dependent conformational perturbations could help to re-establish transcription after mitosis by ‘marking’ genes for re-expression.

Suggested Citation

  • Emil F. Michelotti & Suzanne Sanford & David Levens, 1997. "Marking of active genes on mitotic chromosomes," Nature, Nature, vol. 388(6645), pages 895-899, August.
    • Handle: RePEc:nat:nature:v:388:y:1997:i:6645:d:10.1038_42282
    DOI: 10.1038/42282
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    Cited by:

    1. Rebecca J. Harris & Maninder Heer & Mark D. Levasseur & Tyrell N. Cartwright & Bethany Weston & Jennifer L. Mitchell & Jonathan M. Coxhead & Luke Gaughan & Lisa Prendergast & Daniel Rico & Jonathan M., 2023. "Release of Histone H3K4-reading transcription factors from chromosomes in mitosis is independent of adjacent H3 phosphorylation," Nature Communications, Nature, vol. 14(1), pages 1-17, December.
    2. Sang Bae Lee & Luciano Garofano & Aram Ko & Fulvio D’Angelo & Brulinda Frangaj & Danika Sommer & Qiwen Gan & KyeongJin Kim & Timothy Cardozo & Antonio Iavarone & Anna Lasorella, 2022. "Regulated interaction of ID2 with the anaphase-promoting complex links progression through mitosis with reactivation of cell-type-specific transcription," Nature Communications, Nature, vol. 13(1), pages 1-14, December.

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