Cell
Volume 142, Issue 1, 9 July 2010, Pages 133-143
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Article
TIF1γ Controls Erythroid Cell Fate by Regulating Transcription Elongation

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Summary

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.

Highlights

► Anemia in TIF1γ mutant zebrafish is rescued by loss of transcription pausing factors ► TIF1γ associates with blood transcription factors and pause release factors ► TIF1γ is required for recruiting the pause release factor p-TEFb to erythroid genes

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