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Updated: May 19, 2026

Microbead Implantation in the Zebrafish Embryo

Microbead Implantation in the Zebrafish Embryo

Published on: July 30, 2015

Met regulates endoderm migration in zebrafish.

Po-Shu Tu^1,2, Aaliyah M Ruiz-Corral¹, Stephanie Woo^1,2,3,4

¹Quantitative and Systems Biology Graduate Program, University of California Merced, Merced, California, 95343, USA.

Biorxiv : the Preprint Server for Biology

|May 18, 2026

Summary

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The receptor tyrosine kinase Met promotes persistent, directional cell migration during zebrafish gastrulation. Loss of Met delays development by reducing cell displacement, suggesting a ligand-independent role in regulating cell behavior.

Area of Science:

Developmental Biology
Cell Biology
Molecular Biology

Background:

Cell migration is crucial for development and can occur in different modes.
Receptor tyrosine kinases (RTKs) regulate cell migration, but their in vivo role in shifting migratory behavior is unclear.

Purpose of the Study:

To investigate the role of the RTK Met in regulating endodermal cell migration during zebrafish gastrulation.
To determine if Met signaling influences migratory persistence and directionality in vivo.

Main Methods:

Utilized zebrafish as a model organism.
Employed pharmacological inhibition and genetic loss-of-function of Met.
Performed quantitative live imaging and cell tracking.

Main Results:

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Last Updated: May 19, 2026

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Loss of Met function delayed endoderm convergence by reducing cell displacement and persistence, not velocity.
Met is broadly expressed in migrating endoderm.
Hepatocyte growth factor (Hgf) was dispensable for endoderm convergence.

Conclusions:

Met signaling promotes migratory persistence and directional migration of endodermal cells during gastrulation.
These findings suggest a ligand-independent mechanism for RTK function in regulating developmental cell behaviors.