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TIF1γ Controls Erythroid Cell Fate by Regulating Transcription Elongation

Open access
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.·2010·Cell

Abstract

Summary Recent genome-wide studies have demonstrated 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. ChIP 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.

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Metadata

Authors
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.
Venue
Cell
Publisher
Elsevier BV
Published
2010-07
Volume
142
Issue
1
Pages
133-143
ISSN
0092-8674 (ISSN-L)
OpenAlex
W2011520543
Cited by
212
References
2
FWCI
9.92
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: TIF1γ Controls Erythroid Cell Fate by Regulating Transcription Elongation. https://app.cochat.ai/papers/10.1016/j.cell.2010.05.028
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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. https://doi.org/10.1016/j.cell.2010.05.028

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

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