PUBLICATION

TIF1gamma controls erythroid cell fate by regulating transcription elongation

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., and Zon, L.I.
ID
ZDB-PUB-100719-19
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
Datasets
GEO:GSE20432
MeSH Terms
  • Animals
  • Cell Line, Tumor
  • Cells, Cultured
  • Erythroid Cells/metabolism
  • Erythropoiesis*
  • Humans
  • RNA Polymerase II/metabolism
  • Transcription Factors/metabolism*
  • Transcription, Genetic*
  • Zebrafish/embryology*
  • Zebrafish/metabolism
  • Zebrafish Proteins/metabolism*
PubMed
20603019 Full text @ Cell
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.
Genes / Markers
Figures
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes