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 journalArticle

9 Citations (Scopus)

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.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
JournaleLife
Volume4
Issue numberJUNE
DOIs
Publication statusPublished - Jun 12 2015
Externally publishedYes

Fingerprint

Transcription Factor TFIIIB
Transcription
Chromatin
Histone Code
pol Genes
TATA-Box Binding Protein
Chemical activation
Histones
Genes

ASJC Scopus subject areas

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

Cite this

Lee, Y. L., Li, Y. C., Su, C. H., Chiao, C. H., Lin, I. H., & Hsu, M. T. (2015). MAF1 represses CDKN1A through a Pol III-dependent mechanism. eLife, 4(JUNE), [e06283]. https://doi.org/10.7554/eLife.06283

MAF1 represses CDKN1A through a Pol III-dependent mechanism. / Lee, Yu Ling; Li, Yuan Ching; Su, Chia Hsin; Chiao, Chun Hui; Lin, I. Hsuan; Hsu, Ming Ta.

In: eLife, Vol. 4, No. JUNE, e06283, 12.06.2015.

Research output: Contribution to journalArticle

Lee, YL, Li, YC, Su, CH, Chiao, CH, Lin, IH & Hsu, MT 2015, 'MAF1 represses CDKN1A through a Pol III-dependent mechanism', eLife, vol. 4, no. JUNE, e06283. https://doi.org/10.7554/eLife.06283
Lee YL, Li YC, Su CH, Chiao CH, Lin IH, Hsu MT. MAF1 represses CDKN1A through a Pol III-dependent mechanism. eLife. 2015 Jun 12;4(JUNE). e06283. https://doi.org/10.7554/eLife.06283
Lee, Yu Ling ; Li, Yuan Ching ; Su, Chia Hsin ; Chiao, Chun Hui ; Lin, I. Hsuan ; Hsu, Ming Ta. / MAF1 represses CDKN1A through a Pol III-dependent mechanism. In: eLife. 2015 ; Vol. 4, No. JUNE.
@article{af3c0f4e5f73472e859d1cf431165b9d,
title = "MAF1 represses CDKN1A through a Pol III-dependent mechanism",
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.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.",
author = "Lee, {Yu Ling} and Li, {Yuan Ching} and Su, {Chia Hsin} and Chiao, {Chun Hui} and Lin, {I. Hsuan} and Hsu, {Ming Ta}",
year = "2015",
month = "6",
day = "12",
doi = "10.7554/eLife.06283",
language = "English",
volume = "4",
journal = "eLife",
issn = "2050-084X",
publisher = "eLife Sciences Publications",
number = "JUNE",

}

TY - JOUR

T1 - MAF1 represses CDKN1A through a Pol III-dependent mechanism

AU - Lee, Yu Ling

AU - Li, Yuan Ching

AU - Su, Chia Hsin

AU - Chiao, Chun Hui

AU - Lin, I. Hsuan

AU - Hsu, Ming Ta

PY - 2015/6/12

Y1 - 2015/6/12

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=84933056416&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84933056416&partnerID=8YFLogxK

U2 - 10.7554/eLife.06283

DO - 10.7554/eLife.06283

M3 - Article

VL - 4

JO - eLife

JF - eLife

SN - 2050-084X

IS - JUNE

M1 - e06283

ER -