1. Biochemistry and Chemical Biology
  2. Cell Biology
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MAF1 represses CDKN1A through a Pol III-dependent mechanism

  1. Yu-Ling Lee
  2. Yuan-Ching Li
  3. Chia-Hsin Su
  4. Chun-Hui Chiao
  5. I-Hsuan Lin
  6. Ming-Ta Hsu  Is a corresponding author
  1. National Yang-Ming University, Taiwan
Research Article
  • Cited 13
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Cite this article as: eLife 2015;4:e06283 doi: 10.7554/eLife.06283

Abstract

MAF1 represses Pol III-mediated transcription by interfering with TFIIIB and Pol III. Herein, we found that MAF1 knockdown induced CDKN1A transcription and chromatin looping concurrently with Pol III recruitment. Simultaneous knockdown of MAF1 with Pol III or BRF1 (subunit of TFIIIB) diminished the activation and looping effect, which indicates that recruiting Pol III was required for activation of Pol II-mediated transcription and chromatin looping. ChIP analysis after MAF1 knockdown indicated enhanced binding of Pol III and BRF1, as well as of CFP1, p300, and PCAF, which are factors that mediate active histone marks, along with the binding of TBP and POLR2E to the CDKN1A promoter. Simultaneous knockdown with Pol III abolished these regulatory events. Similar results were obtained for GDF15. Our results reveal a novel mechanism by which MAF1 and Pol III regulate the activity of a protein-coding gene transcribed by Pol II.

Article and author information

Author details

  1. Yu-Ling Lee

    Institute of Biochemistry and Molecular Biology, School of Life Science, National Yang-Ming University, Taipei, Taiwan
    Competing interests
    The authors declare that no competing interests exist.
  2. Yuan-Ching Li

    Institute of Biochemistry and Molecular Biology, School of Life Science, National Yang-Ming University, Taipei, Taiwan
    Competing interests
    The authors declare that no competing interests exist.
  3. Chia-Hsin Su

    Institute of Biochemistry and Molecular Biology, School of Life Science, National Yang-Ming University, Taipei, Taiwan
    Competing interests
    The authors declare that no competing interests exist.
  4. Chun-Hui Chiao

    Institute of Biochemistry and Molecular Biology, School of Life Science, National Yang-Ming University, Taipei, Taiwan
    Competing interests
    The authors declare that no competing interests exist.
  5. I-Hsuan Lin

    Institute of Biochemistry and Molecular Biology, School of Life Science, National Yang-Ming University, Taipei, Taiwan
    Competing interests
    The authors declare that no competing interests exist.
  6. Ming-Ta Hsu

    Institute of Biochemistry and Molecular Biology, School of Life Science, National Yang-Ming University, Taipei, Taiwan
    For correspondence
    mth@ym.edu.tw
    Competing interests
    The authors declare that no competing interests exist.

Reviewing Editor

  1. Joaquín M Espinosa, University of Colorado at Boulder, United States

Publication history

  1. Received: December 29, 2014
  2. Accepted: June 9, 2015
  3. Accepted Manuscript published: June 12, 2015 (version 1)
  4. Version of Record published: June 25, 2015 (version 2)

Copyright

© 2015, Lee et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

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