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Developmental suppression of schizophrenia-associated miR-137 alters sensorimotor function in zebrafish
J Giacomotto1,2, A P Carroll3, S Rinkwitz1
1Brain and Mind Research Institute, Sydney Medical School, University of Sydney, Camperdown, NSW, Australia.
Translational Psychiatry
|May 25, 2016
Summary
MicroRNA miR-137 downregulation impairs zebrafish touch sensitivity. This suggests miR-137 plays a crucial role in sensory neuron development and function, potentially impacting neural connectivity.
Area of Science:
- Neuroscience
- Developmental Biology
- Genetics
Background:
- MicroRNA miR-137 is a risk locus for schizophrenia identified by the Psychiatric Genome Consortium (PGC).
- miR-137 is highly conserved in vertebrates, making zebrafish a suitable model for studying its function.
- Understanding miR-137's role is crucial for insights into neurodevelopmental disorders.
Purpose of the Study:
- To investigate the function of miR-137 in the developing zebrafish nervous system.
- To determine the phenotypic consequences of miR-137 overexpression and suppression.
- To explore the cellular and molecular mechanisms underlying miR-137's effects on sensory function.
Main Methods:
- Utilized zebrafish as a model system for miR-137 functional studies.
- Achieved miR-137 overexpression and suppression using transient and stable transgenesis (miR-sponge RNA).
- Employed antisense morpholino oligonucleotides for miR-137 knockdown.
- Assessed embryonic and larval touch-sensitivity and overall anatomical development.
Main Results:
- miR-137 overexpression did not result in an observable phenotype.
- Downregulation of miR-137 (via morpholino or miR-sponge) significantly impaired embryonic and larval touch-sensitivity.
- No compromise in overall anatomical development was observed following miR-137 downregulation.
- miR-137 expression was detected in sensory neurons, including Rohon-Beard neurons and dorsal root ganglia.
Conclusions:
- miR-137 is essential for normal touch-sensitivity in zebrafish development.
- The observed phenotype is likely due to subtle axonal network defects or altered synaptic function, not gross morphological changes.
- These findings highlight miR-137's critical role in sensory neuron function and neural connectivity, with implications for understanding schizophrenia.
