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Impaired Motor Function in a Zebrafish Stathmin-2 Knockout Model
Tyler J N Gurberg1, Ziyaan A Harji1, Christian J Rampal1
1Department of Neurology and Neurosurgery, Montreal Neurological Institute, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.
Developmental Neurobiology
|July 29, 2026
Summary
We created zebrafish lacking Stathmin-2 (STMN2) genes, revealing impaired motor function and reduced axon regrowth after injury. This highlights STMN2
Area of Science:
- Neuroscience
- Genetics
- Developmental Biology
Background:
- Stathmin-2 (STMN2) is a microtubule-associated protein crucial for axonal stability in the nervous system.
- Understanding STMN2 function is vital for neurodevelopmental and regenerative research.
Purpose of the Study:
- To investigate the role of STMN2 in zebrafish development and motor axon regeneration.
- To characterize a novel zebrafish model lacking both stmn2a and stmn2b genes.
Main Methods:
- Generated a double STMN2 knockout (KO) zebrafish model using CRISPR/Cas9 gene editing.
- Assessed embryonic development, motor function, neuromuscular junction (NMJ) integrity, and axon regeneration capacity.
Main Results:
- The double stmn2a/stmn2b KO zebrafish exhibited increased developmental lethality and impaired embryonic motor function.
- Analysis revealed orphaned NMJs and reduced miniature endplate current amplitude.
- Ventral root axon regrowth following transection was significantly impaired in the KO model.
Conclusions:
- Loss of both stmn2a and stmn2b genes leads to a mild motor phenotype and compromised motor axon regeneration in zebrafish.
- STMN2 plays a role in axonal repair mechanisms following injury.
