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Updated: Mar 21, 2026

The Power of Simplicity: Sea Urchin Embryos as in Vivo Developmental Models for Studying Complex Cell-to-cell Signaling Network Interactions
Published on: February 16, 2017
Terminal alpha-d-mannosides are critical during sea urchin gastrulation
Heghush Aleksanyan1, Jing Liang1, Stan Metzenberg1
1Department of Biology and Center for Cancer and Developmental Biology,California State University,Northridge,California 91330-8303,USA.
High-mannose glycans are crucial for sea urchin embryo gastrulation. Enzyme treatment disrupting these sugars caused developmental defects and impaired cell adhesion, highlighting their role in embryonic development.
Area of Science:
- Developmental Biology
- Glycobiology
- Cell Biology
Background:
- Sea urchin embryos are a model system for studying human health and disease mechanisms.
- High-mannose glycans and polysaccharides play roles in biological processes, including embryonic development.
Purpose of the Study:
- To investigate the role of high-mannose glycans in sea urchin (Lytechinus pictus) gastrulation.
- To determine the effect of α-mannosidase enzyme on embryonic morphology and cell adhesion.
Main Methods:
- Incubation of Lytechinus pictus embryos with Jack bean α-mannosidase.
- Observation of morphological deformations in living embryos.
- Microdissection of fixed embryos to assess archenteron-blastocoel roof adhesion in vitro.
Main Results:
- Enzyme treatment induced significant morphological deformations in developing embryos.
- Even low enzyme activity (0.06 U/ml) caused developmental abnormalities.
- α-mannosidase treatment abrogated the in vitro adhesion of the archenteron tip to the blastocoel roof.
Conclusions:
- Terminal mannose residues are essential for normal gastrulation in sea urchin embryos.
- These residues are involved in the adhesion between the archenteron and blastocoel roof.
- This adhesion may involve a lectin-like mechanism potentially unaffected by fixation.
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