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Related Experiment Video

Updated: Jan 17, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

Published on: June 3, 2018

Rtf1-dependent transcriptional pausing regulates cardiogenesis.

Adam D Langenbacher¹, Fei Lu¹, Luna Tsang¹

¹Department of Molecular, Cell, and Developmental Biology, University of California, Los Angeles, Los Angeles, United States.

|January 15, 2026

Summary

This summary is machine-generated.

Rtf1 protein is crucial for heart development by regulating RNA Polymerase II pausing. Its absence prevents cardiomyocyte formation, but this can be rescued by modulating transcriptional pause release.

Keywords:

PAF1 complex Rtf1 cardiogenesis developmental biology lateral plate mesoderm mouse promoter-proximal pausing transcription regulation zebrafish

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Published on: November 13, 2015

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Last Updated: Jan 17, 2026

Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes

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Published on: June 3, 2018

Assessing Cardiomyocyte Subtypes Following Transcription Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts

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Published on: March 22, 2017

Improved Generation of Induced Cardiomyocytes Using a Polycistronic Construct Expressing Optimal Ratio of Gata4, Mef2c and Tbx5

Improved Generation of Induced Cardiomyocytes Using a Polycistronic Construct Expressing Optimal Ratio of Gata4, Mef2c and Tbx5

Published on: November 13, 2015

Area of Science:

Developmental Biology
Molecular Biology
Genetics

Background:

Transcriptional pause-release is vital for RNA biogenesis.
The role of Rtf1 in embryonic development and heart formation is unclear.

Purpose of the Study:

Investigate Rtf1's function in embryonic heart development.
Determine the molecular mechanisms underlying Rtf1's role in cardiogenesis.

Main Methods:

Utilized zebrafish and mouse models to study Rtf1 function.
Performed structure-function analysis of Rtf1.
Assessed RNA Polymerase II occupancy and CDK9 inhibition.

Main Results:

Rtf1 ablation in zebrafish and mice prevented cardiac progenitor cell formation and cardiomyocyte development.
Rtf1's Plus3 domain is essential for its cardiogenic activity, interacting with Spt5.
Reduced RNA Polymerase II pausing in Rtf1-deficient embryos was observed.
Inhibition of CDK9 restored cardiomyocyte development in Rtf1-deficient embryos.

Conclusions:

Rtf1 is essential for myocardial lineage differentiation and early heart development.
Rtf1 regulates cardiac gene transcription through modulation of RNA Polymerase II pausing.
Targeting transcriptional pause release offers a potential therapeutic strategy for heart development defects.