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

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140 Scopus citations

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 1 2010

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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., LeBlanc, J., Sessa, A., Jiang, H., DiBiase, A., Zhou, Y., Grunwald, D. J., Lin, S., Cantor, A. B., Orkin, S. H., & 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