ZFIN ID: ZDB-PUB-100719-19
TIF1gamma controls erythroid cell fate by regulating transcription elongation
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., and Zon, L.I.
Date: 2010
Source: Cell 142(1): 133-143 (Journal)
Registered Authors: Bai, Xiaoying, DiBiase, Anthony, Grunwald, David, Jiang, Hong, Jurynec, Michael, LeBlanc, Jocelyn, Lin, Shuo, Sessa, Anna, Yang, Zhongan, Zhou, Yi, Zon, Leonard I.
Keywords: DEV BIO, RNA
Microarrays: GEO:GSE20432
MeSH Terms: Animals; Cell Line, Tumor; Cells, Cultured; Erythroid Cells/metabolism; Erythropoiesis* (all 12) expand
PubMed: 20603019 Full text @ Cell
FIGURES   (current status)
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 tif1gamma mutant moonshine we found that loss of function of Pol II-associated factors PAF or DSIF rescued erythroid gene transcription in tif1gamma-deficient animals. Biochemical analysis established physical interactions among TIF1gamma, the blood-specific SCL transcription complex, and the positive elongation factors p-TEFb and FACT. Chromatin immunoprecipitation assays in human CD34(+) cells supported a TIF1gamma-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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