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; Shigetsugu Hatakeyama

doi:10.1038/ncomms6941

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, Shigetsugu Hatakeyama

Research output: Contribution to journal › Article › peer-review

39 Scopus citations

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.

Original language	English (US)
Article number	5941
Journal	Nature communications
Volume	6
DOIs	https://doi.org/10.1038/ncomms6941
State	Published - Jan 9 2015
Externally published	Yes

ASJC Scopus subject areas

Chemistry(all)
Biochemistry, Genetics and Molecular Biology(all)
Physics and Astronomy(all)

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Takahashi, H., Takigawa, I., Watanabe, M., Anwar, D., Shibata, M., Tomomori-Sato, C., Sato, S., Ranjan, A., Seidel, C. W., Tsukiyama, T., Mizushima, W., Hayashi, M., Ohkawa, Y., Conaway, J. W., Conaway, R. C., & Hatakeyama, S. (2015). MED26 regulates the transcription of snRNA genes through the recruitment of little elongation complex. Nature communications, 6, Article 5941. https://doi.org/10.1038/ncomms6941

Takahashi, H, Takigawa, I, Watanabe, M, Anwar, D, Shibata, M, Tomomori-Sato, C, Sato, S, Ranjan, A, Seidel, CW, Tsukiyama, T, Mizushima, W, Hayashi, M, Ohkawa, Y, Conaway, JW, Conaway, RC & Hatakeyama, S 2015, 'MED26 regulates the transcription of snRNA genes through the recruitment of little elongation complex', Nature communications, vol. 6, 5941. https://doi.org/10.1038/ncomms6941

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title = "MED26 regulates the transcription of snRNA genes through the recruitment of little elongation complex",

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.",

author = "Hidehisa Takahashi and Ichigaku Takigawa and Masashi Watanabe and Delnur Anwar and Mio Shibata and Chieri Tomomori-Sato and Shigeo Sato and Amol Ranjan and Seidel, {Chris W.} and Tadasuke Tsukiyama and Wataru Mizushima and Masayasu Hayashi and Yasuyuki Ohkawa and Conaway, {Joan W.} and Conaway, {Ronald C.} and Shigetsugu Hatakeyama",

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AU - Takahashi, Hidehisa

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AU - Shibata, Mio

AU - Tomomori-Sato, Chieri

AU - Sato, Shigeo

AU - Ranjan, Amol

AU - Seidel, Chris W.

AU - Tsukiyama, Tadasuke

AU - Mizushima, Wataru

AU - Hayashi, Masayasu

AU - Ohkawa, Yasuyuki

AU - Conaway, Joan W.

AU - Conaway, Ronald C.

AU - Hatakeyama, Shigetsugu

PY - 2015/1/9

Y1 - 2015/1/9

N2 - 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.

AB - 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.

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

Abstract

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