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

Hidehisa Takahashi, Ichigaku Takigawa, Masashi Watanabe, Delnur Anwar, Mio Shibata, Chieri Tomomori-Sato, Shigeo Sato, Amol Ranjan, Chris W. Seidel, Tadasuke Tsukiyama, Wataru Mizushima, Masayasu Hayashi, Yasuyuki Ohkawa, Joan W. Conaway, Ronald C. Conaway and Shigetsugu Hatakeyama ()
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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
Ronald C. Conaway: Stowers Institute for Medical Research
Shigetsugu Hatakeyama: Hokkaido University Graduate School of Medicine

Nature Communications, 2015, vol. 6, issue 1, 1-15

Abstract: 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.

Date: 2015
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DOI: 10.1038/ncomms6941

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