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MED26 regulates the transcription of snRNA genes through the recruitment of little elongation complex

Author

Listed:
  • Hidehisa Takahashi

    (Hokkaido University Graduate School of Medicine)

  • Ichigaku Takigawa

    (Creative Research Institution, Hokkaido University)

  • Masashi Watanabe

    (Hokkaido University Graduate School of Medicine)

  • Delnur Anwar

    (Hokkaido University Graduate School of Medicine)

  • Mio Shibata

    (Hokkaido University Graduate School of Medicine)

  • Chieri Tomomori-Sato

    (Stowers Institute for Medical Research)

  • Shigeo Sato

    (Stowers Institute for Medical Research)

  • Amol Ranjan

    (Stowers Institute for Medical Research)

  • Chris W. Seidel

    (Stowers Institute for Medical Research)

  • Tadasuke Tsukiyama

    (Hokkaido University Graduate School of Medicine)

  • Wataru Mizushima

    (Hokkaido University Graduate School of Medicine)

  • Masayasu Hayashi

    (Kyushu University Graduate School of Medical Sciences)

  • Yasuyuki Ohkawa

    (Kyushu University Graduate School of Medical Sciences)

  • Joan W. Conaway

    (Stowers Institute for Medical Research
    University of Kansas Medical Center)

  • Ronald C. Conaway

    (Stowers Institute for Medical Research
    University of Kansas Medical Center)

  • Shigetsugu Hatakeyama

    (Hokkaido University Graduate School of Medicine)

Abstract

Regulation of transcription elongation by RNA polymerase II (Pol II) is a key regulatory step in gene transcription. Recently, the little elongation complex (LEC)—which contains the transcription elongation factor ELL/EAF—was found to be required for the transcription of Pol II-dependent small nuclear RNA (snRNA) genes. Here we show that the human Mediator subunit MED26 plays a role in the recruitment of LEC to a subset of snRNA genes through direct interaction of EAF and the N-terminal domain (NTD) of MED26. Loss of MED26 in cells decreases the occupancy of LEC at a subset of snRNA genes and results in a reduction in their transcription. Our results suggest that the MED26-NTD functions as a molecular switch in the exchange of TBP-associated factor 7 (TAF7) for LEC to facilitate the transition from initiation to elongation during transcription of a subset of snRNA genes.

Suggested Citation

  • Hidehisa Takahashi & Ichigaku Takigawa & Masashi Watanabe & Delnur Anwar & Mio Shibata & Chieri Tomomori-Sato & Shigeo Sato & Amol Ranjan & Chris W. Seidel & Tadasuke Tsukiyama & Wataru Mizushima & Ma, 2015. "MED26 regulates the transcription of snRNA genes through the recruitment of little elongation complex," Nature Communications, Nature, vol. 6(1), pages 1-15, May.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms6941
    DOI: 10.1038/ncomms6941
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    Cited by:

    1. Hidefumi Suzuki & Ryota Abe & Miho Shimada & Tomonori Hirose & Hiroko Hirose & Keisuke Noguchi & Yoko Ike & Nanami Yasui & Kazuki Furugori & Yuki Yamaguchi & Atsushi Toyoda & Yutaka Suzuki & Tatsuro Y, 2022. "The 3′ Pol II pausing at replication-dependent histone genes is regulated by Mediator through Cajal bodies’ association with histone locus bodies," Nature Communications, Nature, vol. 13(1), pages 1-24, December.

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