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Updated: Jun 18, 2026
10:12
Differentiation of Human Pluripotent Stem Cells Into Pancreatic Beta-Cell Precursors in a 2D Culture System
Published on: December 16, 2021
SOX9: dosage- and context-dependent functions in pancreatic development and β-cell biology
Nour Sharar1,2, Mohamed Eldaw2, Zeyaul Islam2
1College of Health and Life Sciences, Hamad Bin Khalifa University (HBKU), Qatar Foundation (QF), Doha, P.O. Box 34110, Qatar.
Cell Communication and Signaling : CCS
|June 17, 2026
Summary
SOX9 is crucial for pancreas development and beta-cell function. Its dysregulation causes diabetes-like phenotypes, offering therapeutic targets for preserving beta-cell identity.
Area of Science:
- Endocrinology
- Developmental Biology
- Molecular Biology
Background:
- SOX9 is a conserved transcription factor regulating organogenesis.
- In the pancreas, SOX9 controls progenitor proliferation and endocrine differentiation.
- SOX9's role extends to mature beta-cell function and stress adaptation.
Purpose of the Study:
- To review SOX9's roles in pancreatic development and adult beta-cell biology.
- To highlight conserved mechanisms and species-specific considerations.
- To explore therapeutic opportunities targeting SOX9-dependent pathways.
Main Methods:
- Review of genetic and clinical data from campomelic dysplasia and mouse models.
- Analysis of studies on SOX9 expression and function in pancreatic progenitors and beta-cells.
- Synthesis of current understanding of SOX9's multifaceted roles.
Main Results:
- SOX9 dosage is critical for pancreatic morphogenesis and endocrine formation.
- SOX9 reactivation in adult beta-cells drives dedifferentiation and diabetes-like phenotypes.
- Persistent SOX9 expression in beta-cells regulates splicing and stress adaptation.
Conclusions:
- SOX9 is essential for pancreatic development and lifelong beta-cell function.
- Dysregulated SOX9, particularly rare mutations, impacts pancreatic endocrine formation.
- Targeting SOX9 pathways offers potential for preserving beta-cell function in diabetes.
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