TIF1γ Controls Erythroid Cell Fate by Regulating Transcription Elongation

Xiaoying Bai, Jonghwan Kim, Zhongan Yang, Michael J. Jurynec, Thomas E. Akie, Joseph Lee, Jocelyn LeBlanc, Anna Sessa, Hong Jiang, Anthony DiBiase, Yi Zhou, David J. Grunwald, Shuo Lin, Alan B. Cantor, Stuart H. Orkin, Leonard I. Zon

Research output: Contribution to journalArticle

136 Citations (Scopus)

Abstract

Recent genome-wide studies have demonstrated that pausing of RNA polymerase II (Pol II) occurred on many vertebrate genes. By genetic studies in the zebrafish tif1γ mutant moonshine we found that loss of function of Pol II-associated factors PAF or DSIF rescued erythroid gene transcription in tif1γ-deficient animals. Biochemical analysis established physical interactions among TIF1γ, the blood-specific SCL transcription complex, and the positive elongation factors p-TEFb and FACT. Chromatin immunoprecipitation assays in human CD34+ cells supported a TIF1γ-dependent recruitment of positive elongation factors to erythroid genes to promote transcription elongation by counteracting Pol II pausing. Our study establishes a mechanism for regulating tissue cell fate and differentiation through transcription elongation.

Original languageEnglish (US)
Pages (from-to)133-143
Number of pages11
JournalCell
Volume142
Issue number1
DOIs
StatePublished - Jul 2010

Fingerprint

Erythroid Cells
Transcription
Peptide Elongation Factors
Elongation
Genes
RNA Polymerase II
Chromatin Immunoprecipitation
Zebrafish
Vertebrates
Cell Differentiation
Genome
Chromatin
Assays
Animals
Blood
Tissue
transcriptional intermediary factor 1

Keywords

  • Dev Bio
  • RNA

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Bai, X., Kim, J., Yang, Z., Jurynec, M. J., Akie, T. E., Lee, J., ... Zon, L. I. (2010). TIF1γ Controls Erythroid Cell Fate by Regulating Transcription Elongation. Cell, 142(1), 133-143. https://doi.org/10.1016/j.cell.2010.05.028

TIF1γ Controls Erythroid Cell Fate by Regulating Transcription Elongation. / Bai, Xiaoying; Kim, Jonghwan; Yang, Zhongan; Jurynec, Michael J.; Akie, Thomas E.; Lee, Joseph; LeBlanc, Jocelyn; Sessa, Anna; Jiang, Hong; DiBiase, Anthony; Zhou, Yi; Grunwald, David J.; Lin, Shuo; Cantor, Alan B.; Orkin, Stuart H.; Zon, Leonard I.

In: Cell, Vol. 142, No. 1, 07.2010, p. 133-143.

Research output: Contribution to journalArticle

Bai, X, Kim, J, Yang, Z, Jurynec, MJ, Akie, TE, Lee, J, LeBlanc, J, Sessa, A, Jiang, H, DiBiase, A, Zhou, Y, Grunwald, DJ, Lin, S, Cantor, AB, Orkin, SH & Zon, LI 2010, 'TIF1γ Controls Erythroid Cell Fate by Regulating Transcription Elongation', Cell, vol. 142, no. 1, pp. 133-143. https://doi.org/10.1016/j.cell.2010.05.028
Bai X, Kim J, Yang Z, Jurynec MJ, Akie TE, Lee J et al. TIF1γ Controls Erythroid Cell Fate by Regulating Transcription Elongation. Cell. 2010 Jul;142(1):133-143. https://doi.org/10.1016/j.cell.2010.05.028
Bai, Xiaoying ; Kim, Jonghwan ; Yang, Zhongan ; Jurynec, Michael J. ; Akie, Thomas E. ; Lee, Joseph ; LeBlanc, Jocelyn ; Sessa, Anna ; Jiang, Hong ; DiBiase, Anthony ; Zhou, Yi ; Grunwald, David J. ; Lin, Shuo ; Cantor, Alan B. ; Orkin, Stuart H. ; Zon, Leonard I. / TIF1γ Controls Erythroid Cell Fate by Regulating Transcription Elongation. In: Cell. 2010 ; Vol. 142, No. 1. pp. 133-143.
@article{d335ed520cf247f686e24d8c875707f1,
title = "TIF1γ Controls Erythroid Cell Fate by Regulating Transcription Elongation",
abstract = "Recent genome-wide studies have demonstrated that pausing of RNA polymerase II (Pol II) occurred on many vertebrate genes. By genetic studies in the zebrafish tif1γ mutant moonshine we found that loss of function of Pol II-associated factors PAF or DSIF rescued erythroid gene transcription in tif1γ-deficient animals. Biochemical analysis established physical interactions among TIF1γ, the blood-specific SCL transcription complex, and the positive elongation factors p-TEFb and FACT. Chromatin immunoprecipitation assays in human CD34+ cells supported a TIF1γ-dependent recruitment of positive elongation factors to erythroid genes to promote transcription elongation by counteracting Pol II pausing. Our study establishes a mechanism for regulating tissue cell fate and differentiation through transcription elongation.",
keywords = "Dev Bio, RNA",
author = "Xiaoying Bai and Jonghwan Kim and Zhongan Yang and Jurynec, {Michael J.} and Akie, {Thomas E.} and Joseph Lee and Jocelyn LeBlanc and Anna Sessa and Hong Jiang and Anthony DiBiase and Yi Zhou and Grunwald, {David J.} and Shuo Lin and Cantor, {Alan B.} and Orkin, {Stuart H.} and Zon, {Leonard I.}",
year = "2010",
month = "7",
doi = "10.1016/j.cell.2010.05.028",
language = "English (US)",
volume = "142",
pages = "133--143",
journal = "Cell",
issn = "0092-8674",
publisher = "Cell Press",
number = "1",

}

TY - JOUR

T1 - TIF1γ Controls Erythroid Cell Fate by Regulating Transcription Elongation

AU - Bai, Xiaoying

AU - Kim, Jonghwan

AU - Yang, Zhongan

AU - Jurynec, Michael J.

AU - Akie, Thomas E.

AU - Lee, Joseph

AU - LeBlanc, Jocelyn

AU - Sessa, Anna

AU - Jiang, Hong

AU - DiBiase, Anthony

AU - Zhou, Yi

AU - Grunwald, David J.

AU - Lin, Shuo

AU - Cantor, Alan B.

AU - Orkin, Stuart H.

AU - Zon, Leonard I.

PY - 2010/7

Y1 - 2010/7

N2 - Recent genome-wide studies have demonstrated that pausing of RNA polymerase II (Pol II) occurred on many vertebrate genes. By genetic studies in the zebrafish tif1γ mutant moonshine we found that loss of function of Pol II-associated factors PAF or DSIF rescued erythroid gene transcription in tif1γ-deficient animals. Biochemical analysis established physical interactions among TIF1γ, the blood-specific SCL transcription complex, and the positive elongation factors p-TEFb and FACT. Chromatin immunoprecipitation assays in human CD34+ cells supported a TIF1γ-dependent recruitment of positive elongation factors to erythroid genes to promote transcription elongation by counteracting Pol II pausing. Our study establishes a mechanism for regulating tissue cell fate and differentiation through transcription elongation.

AB - Recent genome-wide studies have demonstrated that pausing of RNA polymerase II (Pol II) occurred on many vertebrate genes. By genetic studies in the zebrafish tif1γ mutant moonshine we found that loss of function of Pol II-associated factors PAF or DSIF rescued erythroid gene transcription in tif1γ-deficient animals. Biochemical analysis established physical interactions among TIF1γ, the blood-specific SCL transcription complex, and the positive elongation factors p-TEFb and FACT. Chromatin immunoprecipitation assays in human CD34+ cells supported a TIF1γ-dependent recruitment of positive elongation factors to erythroid genes to promote transcription elongation by counteracting Pol II pausing. Our study establishes a mechanism for regulating tissue cell fate and differentiation through transcription elongation.

KW - Dev Bio

KW - RNA

UR - http://www.scopus.com/inward/record.url?scp=77954301966&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=77954301966&partnerID=8YFLogxK

U2 - 10.1016/j.cell.2010.05.028

DO - 10.1016/j.cell.2010.05.028

M3 - Article

C2 - 20603019

AN - SCOPUS:77954301966

VL - 142

SP - 133

EP - 143

JO - Cell

JF - Cell

SN - 0092-8674

IS - 1

ER -