Summary
Published in Diabetologia (2025), this peer-reviewed study used 3D Petri Dish® micro-molds to form scaffold-free 3D microtissues. Full citation: Kobaisi, Farah, et al. MNX1 prevents somatostatin expression in human beta cells by repressing PERCC1
MNX1 prevents somatostatin expression in human beta cells by repressing PERCC1
Research Overview
A precise mosaic of transcription factors guides pancreatic progenitors and maintains the identity of mature endocrine cells. In mice, MNX1 is essential for β-cell development and identity — deleting it in mature β-cells increases somatostatin expression through an unknown mechanism. This study asked whether MNX1 plays the same role in human β-cells and which molecular players are involved.
Using the human β-cell line EndoC-βH1, the authors knocked down MNX1 with siRNA and performed bulk RNA sequencing to find its targets, then ran loss-of-function (siRNA) and gain-of-function (lentiviral and lipofection) experiments to determine how MNX1 regulates gene expression and guards β-cell identity against the somatostatin program.
Key Discoveries
- MNX1 knockdown in human EndoC-βH1 β-cells profiled by bulk RNA-seq to identify targets
- Loss- and gain-of-function experiments dissected how MNX1 regulates downstream genes
- Extends the mouse finding that MNX1 restrains somatostatin expression to human β-cells
