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Assessing Cardiomyocyte Subtypes Following Transcription Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts
Published on: March 22, 2017
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Genome-wide transcriptomics analysis identifies sox7 and sox18 as specifically regulated by gata4 in cardiomyogenesis
Boni A Afouda1, Adam T Lynch1, Eduardo de Paiva Alves2
1Institute of Medical Sciences, Foresterhill Health Campus, University of Aberdeen, Scotland, UK.
Developmental Biology
|December 13, 2017
Summary
GATA4 is crucial for heart muscle development. This study reveals a conserved pathway where GATA4 regulates SOX7 and SOX18, essential for cardiomyogenesis.
Area of Science:
- Cardiovascular Biology
- Developmental Biology
- Gene Regulation
Background:
- GATA4, GATA5, and GATA6 are key regulators of heart muscle differentiation (cardiomyogenesis).
- These factors exhibit partial functional redundancy.
- GATA4 is particularly potent in inducing cardiomyocyte differentiation.
Purpose of the Study:
- To identify genes specifically regulated by individual cardiogenic GATA factors.
- To investigate the role of GATA4-regulated genes in cardiomyogenesis.
- To determine the conserved function of the GATA4-SoxF axis in mammalian heart development.
Main Methods:
- Genome-wide transcriptomics analysis to identify GATA-factor-specific targets.
- Gene knockdown and experimental reinstatement in Xenopus and mouse embryonic stem cells (ESCs).
- Assessment of cardiomyocyte differentiation and gene expression changes.
Main Results:
- GATA4 specifically regulates SoxF family members, sox7 and sox18.
- Restoring GATA4 expression re-establishes sox7 and sox18 levels.
- Overexpression of sox7 or sox18 partially rescues cardiomyocyte differentiation defects caused by GATA4 knockdown.
- Gata4 knockdown reduces Sox7 and Sox18 expression in mouse ESCs, and Gata4 induces Sox7 expression.
Conclusions:
- A conserved gene regulatory axis exists from GATA4 to SoxF paralogs (sox7 and sox18).
- This GATA4-SoxF axis is critical for heart muscle cell differentiation.
- GATA4 plays a unique and essential role in initiating cardiomyogenesis through SOXF factors.
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