MAF1 represses CDKN1A through a Pol III-dependent mechanism

Yu Ling Lee, Yuan Ching Li, Chia Hsin Su, Chun Hui Chiao, I. Hsuan Lin, Ming Ta Hsu

Research output: Contribution to journalArticlepeer-review

15 Citations (Scopus)


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.Chromatinimmunoprecipitation 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 TATA binding protein (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 proteincoding gene transcribed by Pol II.

Original languageEnglish
Article numbere06283
Issue numberJUNE
Publication statusPublished - Jun 12 2015
Externally publishedYes

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)


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