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Updated: Aug 21, 2026

Visualizing the Node and Notochordal Plate In Gastrulating Mouse Embryos Using Scanning Electron Microscopy and Whole Mount Immunofluorescence
Published on: November 6, 2018
The activity of the Nodal antagonist Cerl-2 in the mouse node is required for correct L/R body axis
Sara Marques1, Ana Cristina Borges, Ana Cristina Silva
1Instituto Gulbenkian de Ciência, 2781-901 Oeiras, Portugal.
Insights
Cerl-2, a Nodal antagonist, is crucial for establishing left/right body asymmetry in mouse embryos. Its asymmetric expression prevents Nodal signaling on the right, ensuring proper embryonic development and laterality.
Area of Science:
- Developmental Biology
- Genetics
- Molecular Biology
Background:
- Left/right (L/R) body asymmetry is vital for embryonic development.
- The Nodal signaling pathway is conserved and essential for establishing L/R asymmetry.
- Nodal expression in the left lateral plate mesoderm (L-LPM) is critical, dependent on Nodal presence in the node.
Purpose of the Study:
- To characterize the function of cerl-2, a novel Nodal antagonist.
- To investigate the role of cerl-2 in L/R body asymmetry.
- To understand how cerl-2 restricts Nodal signaling during embryonic development.
Main Methods:
- Characterization of cerl-2 function.
- Analysis of cerl-2 knockout mouse models.
- Genetic manipulation involving Nodal alleles.
Main Results:
- Cerl-2 exhibits asymmetric expression on the right side of the mouse node.
- Cerl-2 knockout mice display significant laterality defects, including randomized L/R axis.
- Partial rescue of defects was observed when one Nodal allele was removed.
Conclusions:
- Cerl-2 is a key regulator of L/R body asymmetry in mouse embryos.
- Cerl-2 restricts Nodal signaling to the left side by inhibiting its activity on the right.
- Understanding cerl-2 function provides insights into the molecular mechanisms of embryonic asymmetry.
Abstract:
Correct establishment of the left/right (L/R) body asymmetry in the mouse embryo requires asymmetric activation of the evolutionarily conserved Nodal signaling cascade in the left lateral plate mesoderm (L-LPM). Furthermore, the presence of Nodal in the node is essential for its own expression in the L-LPM. Here, we have characterized the function of cerl-2, a novel Nodal antagonist, which displays a unique asymmetric expression on the right side of the mouse node. cerl-2 knockout mice display multiple laterality defects including randomization of the L/R axis. These defects can be partially rescued by removing one nodal allele. Our results demonstrate that Cerl-2 plays a key role in restricting the Nodal signaling pathway toward the left side of the mouse embryo by preventing its activity in the right side.
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