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Related Experiment Video

Updated: Apr 24, 2026

Isolation and Culture of Cells from the Nephrogenic Zone of the Embryonic Mouse Kidney

Isolation and Culture of Cells from the Nephrogenic Zone of the Embryonic Mouse Kidney

Published on: April 22, 2011

A regulatory network controls nephrocan expression and midgut patterning.

Juan Hou¹, Wei Wei¹, Ranajeet S Saund²

¹Terry Fox Laboratory, BC Cancer Agency, Vancouver, British Columbia, V5Z 1L3, Canada.

Development (Cambridge, England)

|September 12, 2014

Summary

Sox17 and retinoic acid signaling establish midgut gene expression. Nodal and Activin signaling further refine this domain, revealing key mechanisms in gut development.

Keywords:

Midgut definitive endoderm Mouse Nephrocan (Nepn)Nodal/Activin A Retinoic acid Sox17

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Area of Science:

Developmental Biology
Genetics
Molecular Biology

Background:

Understanding endoderm development is crucial for regenerative medicine and disease research.
Mechanisms of midgut patterning remain incompletely understood.
Nephrocan (Nepn) is the earliest known midgut-specific gene in mice.

Purpose of the Study:

To investigate the transcriptional regulatory mechanisms controlling midgut patterning.
To dissect the regulatory elements of the nephrocan (Nepn) gene.

Main Methods:

Gene expression analysis in knockout mouse embryos (Sox17-/-, Raldh2-/-, Foxh1-/-).
Identification and characterization of enhancer elements.
Assessment of signaling pathway modulation (Activin, Nodal, Retinoic Acid).

Main Results:

Nepn expression is dependent on Sox17 and retinoic acid (RA) signaling via upstream enhancers.
Activin signaling inversely modulates RA-dependent Nepn expression.
Nodal signaling restricts the anterior boundary of Nepn expression in vivo.

Conclusions:

Sox17 is essential for Nepn expression in the definitive endoderm.
RA signaling restricts Nepn expression to the midgut region.
A balance of Nodal/Activin signaling defines the anterior midgut boundary.