Developmental suppression of schizophrenia-associated miR-137 alters sensorimotor function in zebrafish

Giacomotto, J., Carroll, A. P., Rinkwitz, S., Mowry, B., Cairns, M. J. and Becker, T. S. (2016) Developmental suppression of schizophrenia-associated miR-137 alters sensorimotor function in zebrafish. Translational Psychiatry, 6 1-10. doi:10.1038/tp.2016.88


Author Giacomotto, J.
Carroll, A. P.
Rinkwitz, S.
Mowry, B.
Cairns, M. J.
Becker, T. S.
Title Developmental suppression of schizophrenia-associated miR-137 alters sensorimotor function in zebrafish
Journal name Translational Psychiatry   Check publisher's open access policy
ISSN 2158-3188
Publication date 2016-05-24
Sub-type Article (original research)
DOI 10.1038/tp.2016.88
Open Access Status DOI
Volume 6
Start page 1
End page 10
Total pages 10
Place of publication London, United Kingdom
Publisher Nature Publishing Group
Collection year 2017
Language eng
Abstract The neurodevelopmentally regulated microRNA miR-137 was strongly implicated as risk locus for schizophrenia in the most recent genome wide association study coordinated by the Psychiatric Genome Consortium (PGC). This molecule is highly conserved in vertebrates enabling the investigation of its function in the developing zebrafish. We utilized this model system to achieve overexpression and suppression of miR-137, both transiently and stably through transgenesis. While miR-137 overexpression was not associated with an observable specific phenotype, downregulation by antisense morpholino and/or transgenic expression of miR-sponge RNA induced significant impairment of both embryonic and larval touch-sensitivity without compromising overall anatomical development. We observed miR-137 expression and activity in sensory neurons including Rohon–Beard neurons and dorsal root ganglia, two neuronal cell types that confer touch-sensitivity in normal zebrafish, suggesting a role of these cell types in the observed phenotype. The lack of obvious anatomical or histological pathology in these cells, however, suggested that subtle axonal network defects or a change in synaptic function and neural connectivity might be responsible for the behavioral phenotype rather than a change in the cellular morphology or neuroanatomy.
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status UQ
Additional Notes Article number e818

Document type: Journal Article
Sub-type: Article (original research)
Collections: HERDC Pre-Audit
Queensland Brain Institute Publications
 
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Created: Tue, 07 Jun 2016, 20:27:06 EST by Jean Giacomotto on behalf of Queensland Brain Institute