The role of Mediator and Little Elongation Complex in transcription termination

Hidehisa Takahashi; Amol Ranjan; Shiyuan Chen; Hidefumi Suzuki; Mio Shibata; Tomonori Hirose; Hiroko Hirose; Kazunori Sasaki; Ryota Abe; Kai Chen; Yanfeng He; Ying Zhang; Ichigaku Takigawa; Tadasuke Tsukiyama; Masashi Watanabe; Satoshi Fujii; Midori Iida; Junichi Yamamoto; Yuki Yamaguchi; Yutaka Suzuki; Masaki Matsumoto; Keiichi I. Nakayama; Michael P. Washburn; Anita Saraf; Laurence Florens; Shigeo Sato; Chieri Tomomori-Sato; Ronald C. Conaway; Joan W. Conaway; Shigetsugu Hatakeyama

doi:10.1038/s41467-020-14849-1

The role of Mediator and Little Elongation Complex in transcription termination

Hidehisa Takahashi, Amol Ranjan, Shiyuan Chen, Hidefumi Suzuki, Mio Shibata, Tomonori Hirose, Hiroko Hirose, Kazunori Sasaki, Ryota Abe, Kai Chen, Yanfeng He, Ying Zhang, Ichigaku Takigawa, Tadasuke Tsukiyama, Masashi Watanabe, Satoshi Fujii, Midori Iida, Junichi Yamamoto, Yuki Yamaguchi, Yutaka SuzukiMasaki Matsumoto, Keiichi I. Nakayama, Michael P. Washburn, Anita Saraf, Laurence Florens, Shigeo Sato, Chieri Tomomori-Sato, Ronald C. Conaway, Joan W. Conaway, Shigetsugu Hatakeyama

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

20 Scopus citations

Abstract

Mediator is a coregulatory complex that regulates transcription of Pol II-dependent genes. Previously, we showed that human Mediator subunit MED26 plays a role in the recruitment of Super Elongation Complex (SEC) or Little Elongation Complex (LEC) to regulate the expression of certain genes. MED26 plays a role in recruiting SEC to protein-coding genes including c-myc and LEC to small nuclear RNA (snRNA) genes. However, how MED26 engages SEC or LEC to regulate distinct genes is unclear. Here, we provide evidence that MED26 recruits LEC to modulate transcription termination of non-polyadenylated transcripts including snRNAs and mRNAs encoding replication-dependent histone (RDH) at Cajal bodies. Our findings indicate that LEC recruited by MED26 promotes efficient transcription termination by Pol II through interaction with CBC-ARS2 and NELF/DSIF, and promotes 3′ end processing by enhancing recruitment of Integrator or Heat Labile Factor to snRNA or RDH genes, respectively.

Original language	English (US)
Article number	1063
Journal	Nature communications
Volume	11
Issue number	1
DOIs	https://doi.org/10.1038/s41467-020-14849-1
State	Published - Dec 1 2020
Externally published	Yes

ASJC Scopus subject areas

General Chemistry
General Biochemistry, Genetics and Molecular Biology
General Physics and Astronomy

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Takahashi, H., Ranjan, A., Chen, S., Suzuki, H., Shibata, M., Hirose, T., Hirose, H., Sasaki, K., Abe, R., Chen, K., He, Y., Zhang, Y., Takigawa, I., Tsukiyama, T., Watanabe, M., Fujii, S., Iida, M., Yamamoto, J., Yamaguchi, Y., ... Hatakeyama, S. (2020). The role of Mediator and Little Elongation Complex in transcription termination. Nature communications, 11(1), Article 1063. https://doi.org/10.1038/s41467-020-14849-1

Takahashi, H, Ranjan, A, Chen, S, Suzuki, H, Shibata, M, Hirose, T, Hirose, H, Sasaki, K, Abe, R, Chen, K, He, Y, Zhang, Y, Takigawa, I, Tsukiyama, T, Watanabe, M, Fujii, S, Iida, M, Yamamoto, J, Yamaguchi, Y, Suzuki, Y, Matsumoto, M, Nakayama, KI, Washburn, MP, Saraf, A, Florens, L, Sato, S, Tomomori-Sato, C, Conaway, RC, Conaway, JW & Hatakeyama, S 2020, 'The role of Mediator and Little Elongation Complex in transcription termination', Nature communications, vol. 11, no. 1, 1063. https://doi.org/10.1038/s41467-020-14849-1

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abstract = "Mediator is a coregulatory complex that regulates transcription of Pol II-dependent genes. Previously, we showed that human Mediator subunit MED26 plays a role in the recruitment of Super Elongation Complex (SEC) or Little Elongation Complex (LEC) to regulate the expression of certain genes. MED26 plays a role in recruiting SEC to protein-coding genes including c-myc and LEC to small nuclear RNA (snRNA) genes. However, how MED26 engages SEC or LEC to regulate distinct genes is unclear. Here, we provide evidence that MED26 recruits LEC to modulate transcription termination of non-polyadenylated transcripts including snRNAs and mRNAs encoding replication-dependent histone (RDH) at Cajal bodies. Our findings indicate that LEC recruited by MED26 promotes efficient transcription termination by Pol II through interaction with CBC-ARS2 and NELF/DSIF, and promotes 3′ end processing by enhancing recruitment of Integrator or Heat Labile Factor to snRNA or RDH genes, respectively.",

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AU - Chen, Shiyuan

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AU - Shibata, Mio

AU - Hirose, Tomonori

AU - Hirose, Hiroko

AU - Sasaki, Kazunori

AU - Abe, Ryota

AU - Chen, Kai

AU - He, Yanfeng

AU - Zhang, Ying

AU - Takigawa, Ichigaku

AU - Tsukiyama, Tadasuke

AU - Watanabe, Masashi

AU - Fujii, Satoshi

AU - Iida, Midori

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AU - Yamaguchi, Yuki

AU - Suzuki, Yutaka

AU - Matsumoto, Masaki

AU - Nakayama, Keiichi I.

AU - Washburn, Michael P.

AU - Saraf, Anita

AU - Florens, Laurence

AU - Sato, Shigeo

AU - Tomomori-Sato, Chieri

AU - Conaway, Ronald C.

AU - Conaway, Joan W.

AU - Hatakeyama, Shigetsugu

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N2 - Mediator is a coregulatory complex that regulates transcription of Pol II-dependent genes. Previously, we showed that human Mediator subunit MED26 plays a role in the recruitment of Super Elongation Complex (SEC) or Little Elongation Complex (LEC) to regulate the expression of certain genes. MED26 plays a role in recruiting SEC to protein-coding genes including c-myc and LEC to small nuclear RNA (snRNA) genes. However, how MED26 engages SEC or LEC to regulate distinct genes is unclear. Here, we provide evidence that MED26 recruits LEC to modulate transcription termination of non-polyadenylated transcripts including snRNAs and mRNAs encoding replication-dependent histone (RDH) at Cajal bodies. Our findings indicate that LEC recruited by MED26 promotes efficient transcription termination by Pol II through interaction with CBC-ARS2 and NELF/DSIF, and promotes 3′ end processing by enhancing recruitment of Integrator or Heat Labile Factor to snRNA or RDH genes, respectively.

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The role of Mediator and Little Elongation Complex in transcription termination

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