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An Optimized Protocol for Electrophoretic Mobility Shift Assay Using Infrared Fluorescent Dye-labeled Oligonucleotides

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EPHA2 Regulates SOX2 during Esophageal Development.

Tianxia Li, Yosuke Mitani, Ricardo Cruz-Acuña

Biorxiv : the Preprint Server for Biology

|October 17, 2024

Summary

This summary is machine-generated.

The receptor tyrosine kinase EPHA2 regulates SOX2 expression during human esophageal development. Inhibiting EPHA2 impaired esophageal organoid formation and SOX2 levels, highlighting EPHA2

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A Rapid In Vivo Bioassay for Developmentally Active Enhancers

A Rapid In Vivo Bioassay for Developmentally Active Enhancers

Area of Science:

Developmental Biology
Stem Cell Biology
Molecular Biology

Background:

Proper dorsal-ventral patterning of the anterior foregut endoderm is essential for human esophageal development.
The transcription factor SOX2 plays a critical role in esophageal development, and its dysregulation is linked to congenital abnormalities.
EPHA2, a receptor tyrosine kinase, is implicated in developmental processes and cancer, where it has been shown to activate SOX2.

Purpose of the Study:

To investigate the role of EPHA2 in regulating SOX2 expression during human esophageal development.
To determine the impact of EPHA2 inhibition on human esophageal organoid formation and SOX2 signaling.

Main Methods:

Utilized human induced pluripotent stem cells (iPSCs).
Generated and analyzed human esophageal organoids (HEOs) derived from iPSCs.
Assessed the effects of EPHA2 inhibition on HEO formation and SOX2 expression.

Main Results:

EPHA2 was demonstrated to regulate SOX2 expression in developing human esophageal organoids.
Inhibition of EPHA2 led to a decrease in the formation of iPSC-derived HEOs.
EPHA2 inhibition also resulted in reduced SOX2 expression within the developing organoids.

Conclusions:

EPHA2 acts as a key regulator of SOX2 signaling during early human esophageal development.
These findings establish a novel link between EPHA2 and SOX2 in the context of esophageal organogenesis.
The study provides insights into the molecular mechanisms underlying congenital esophageal abnormalities.