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HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes

Author

Listed:
  • Alison K. Barrett

    (University of California)

  • Manisha R. Shingare

    (University of California)

  • Andreas Rechtsteiner

    (University of California)

  • Kelsie M. Rodriguez

    (University of California)

  • Quynh N. Le

    (University of California)

  • Tilini U. Wijeratne

    (University of California)

  • Corbin E. Mitchell

    (University of California)

  • Miles W. Membreno

    (University of California)

  • Seth M. Rubin

    (University of California)

  • Gerd A. Müller

    (University of California)

Abstract

Histone deacetylases (HDACs) play a crucial role in transcriptional regulation and are implicated in various diseases, including cancer. They are involved in histone tail deacetylation and canonically linked to transcriptional repression. Previous studies suggested that HDAC recruitment to cell-cycle gene promoters via the retinoblastoma (RB) protein or the DREAM complex through SIN3B is essential for G1/S and G2/M gene repression during cell-cycle arrest and exit. Here we investigate the interplay among DREAM, RB, SIN3 proteins, and HDACs in the context of cell-cycle gene repression. Knockout of SIN3B does not globally derepress cell-cycle genes in non-proliferating HCT116 and C2C12 cells. Loss of SIN3A/B moderately upregulates several cell-cycle genes in HCT116 cells but does so independently of DREAM/RB. HDAC inhibition does not induce general upregulation of RB/DREAM target genes in arrested transformed or non-transformed cells. Our findings suggest that E2F:RB and DREAM complexes can repress cell-cycle genes without relying on HDAC activity.

Suggested Citation

  • Alison K. Barrett & Manisha R. Shingare & Andreas Rechtsteiner & Kelsie M. Rodriguez & Quynh N. Le & Tilini U. Wijeratne & Corbin E. Mitchell & Miles W. Membreno & Seth M. Rubin & Gerd A. Müller, 2024. "HDAC activity is dispensable for repression of cell-cycle genes by DREAM and E2F:RB complexes," Nature Communications, Nature, vol. 15(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-48724-0
    DOI: 10.1038/s41467-024-48724-0
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    References listed on IDEAS

    as
    1. Marios G. Koliopoulos & Reyhan Muhammad & Theodoros I. Roumeliotis & Fabienne Beuron & Jyoti S. Choudhary & Claudio Alfieri, 2022. "Structure of a nucleosome-bound MuvB transcription factor complex reveals DNA remodelling," Nature Communications, Nature, vol. 13(1), pages 1-14, December.
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    4. Anushweta Asthana & Parameshwaran Ramanan & Alexander Hirschi & Keelan Z. Guiley & Tilini U. Wijeratne & Robert Shelansky & Michael J. Doody & Haritha Narasimhan & Hinrich Boeger & Sarvind Tripathi & , 2022. "The MuvB complex binds and stabilizes nucleosomes downstream of the transcription start site of cell-cycle dependent genes," Nature Communications, Nature, vol. 13(1), pages 1-15, December.
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