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Related Experiment Video

Updated: Feb 24, 2026

Mouse Fetal Whole Intestine Culture System for Ex Vivo Manipulation of Signaling Pathways and Three-dimensional Live Imaging of Villus Development

Mouse Fetal Whole Intestine Culture System for Ex Vivo Manipulation of Signaling Pathways and Three-dimensional Live Imaging of Villus Development

Published on: September 4, 2014

Absence of EOGT Precludes Defective Development in Fringe-null Mouse Intestine.

Mohd Nauman, Pamela Stanley

Biorxiv : the Preprint Server for Biology

|February 23, 2026

Summary

This summary is machine-generated.

Altering Fringe glycosyltransferase activity in the intestine disrupts development, increasing goblet and Paneth cells. However, the absence of EOGT prevents these defects, revealing EOGT

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Area of Science:

Biochemistry
Developmental Biology
Cell Biology

Background:

Glycosyltransferases play crucial roles in cellular processes, and understanding their function is vital for congenital disorders of glycosylation.
Notch signaling, essential for development, relies on specific O-glycans on epidermal growth factor-like (EGF) repeats, modified by Fringe enzymes and EOGT.
Previous studies linked O-fucosylation defects to intestinal developmental issues.

Purpose of the Study:

To investigate the impact of Fringe glycosyltransferases (LFNG, MFNG, RFNG) and EOGT on intestinal development.
To determine if inhibiting Fringe activity alone or in combination affects intestinal morphology.
To explore the interplay between Fringe enzymes and EOGT in regulating intestinal development.

Main Methods:

Conditional gene deletion of Fringe genes (Lfng, Mfng, Rfng) in mouse intestinal epithelium using Villin-Cre.
Generation of mice with combined Fringe gene inactivation and EOGT deficiency.
Analysis of intestinal morphology, including cell type composition (goblet, Paneth cells) and tissue architecture (villus length, crypt width).

Main Results:

Conditional deletion of Lfng alone or all three Fringe genes resulted in defective intestinal development, characterized by increased goblet and Paneth cells, wider crypts, and shorter villi.
Unexpectedly, in mice lacking EOGT, the inactivation of Fringe genes did not cause intestinal developmental defects.
The absence of EOGT appeared to protect the intestine from the disruptive effects of Fringe gene inactivation.

Conclusions:

Fringe glycosyltransferases are essential for normal intestinal development.
EOGT plays a critical, previously unrecognized role in regulating intestinal development, potentially by modulating Fringe-mediated O-glycosylation.
The findings reveal a novel regulatory mechanism involving EOGT in intestinal development and Notch signaling pathways.