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Aagab is required for zebrafish larval development by regulating neural activity.
Shihui Ding1, Tursunjan Aziz1, Anming Meng2
1State Key Laboratory of Membrane Biology, Tsinghua-Peking Center for Life Sciences, School of Life Sciences, Tsinghua University, Beijing 100084, China.
Journal of Genetics and Genomics = Yi Chuan Xue Bao
|January 22, 2024
Summary
The study reveals that the α- and γ-adaptin binding protein (Aagab) is crucial for zebrafish nervous system function, impacting neurotransmitter release and synaptic vesicle recycling. Aagab deficiency leads to neurological deficits and reduced survival.
Area of Science:
- Neurobiology
- Cell Biology
- Developmental Biology
Background:
- Clathrin-mediated endocytosis is vital for numerous cellular processes.
- The physiological role of α- and γ-adaptin binding protein (Aagab) in endocytosis remains unclear.
Purpose of the Study:
- To investigate the biological function of Aagab in zebrafish development and the nervous system.
- To elucidate the role of Aagab in synaptic vesicle recycling and neurotransmission.
Main Methods:
- Generation of aagab loss-of-function zebrafish mutants.
- Assessment of swimming behavior, survival rates, and neurological function (calcium responses, local field potentials).
- Analysis of neurotransmitter release and FM 1-43 dye uptake in neuroblastoma cells.
Main Results:
- aagab mutants exhibit impaired swimming, reduced survival, and subdued neuronal activity in the optic tectum.
- Mutants show decreased norepinephrine release and delayed synaptic vesicle recycling.
- Overexpression of Aagab or nervous stimulant treatment rescues these deficits.
Conclusions:
- Aagab plays a significant role in zebrafish neurobiology, particularly in synaptic vesicle recycling and neurotransmission.
- Aagab deficiency impacts neuronal function and survival, suggesting potential implications for neurological disorders.
