ArticlePLoS genetics2011
Celsr3 is required for normal development of GABA circuits in the inner retina.
Article in PLoS genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 29 citations in OpenAlex.
- Adhesion G protein-coupled receptors.Pharmacological reviews · 2026Review
- Adhesion G-Protein Coupled Receptors in Neurological and Psychiatric Disorders.Journal of psychiatry and brain science · 2025Article
- Experience-dependent, sexually dimorphic synaptic connectivity defined by sex-specific cadherin expression.Science advances · 2024Article
- Experience-dependent, sexually dimorphic synaptic connectivity defined by sex-specific cadherin expression.bioRxiv : the preprint server for biology · 2024Article
- Assessing Rewiring of the Retinal Circuitry by Electroretinogram (ERG) After Inner Retinal Lesion in Adult Zebrafish.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Zebrafish models of alx-linked frontonasal dysplasia reveal a role for Alx1 and Alx3 in the anterior segment and vasculature of the developing eye.Biology open · 2022Article
- Review
- Identification of Possible Risk Variants of Familial Strabismus Using Exome Sequencing Analysis.Genes · 2021Observational
- Pregnancy-Associated Plasma Protein-aa Regulates Photoreceptor Synaptic Development to Mediate Visually Guided Behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Cone signals in monostratified and bistratified amacrine cells of adult zebrafish retina.The Journal of comparative neurology · 2017Article
- Evidence for opposing roles of Celsr3 and Vangl2 in glutamatergic synapse formation.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- APLP2 Regulates Refractive Error and Myopia Development in Mice and Humans.PLoS genetics · 2015Article
- Electroretinogram analysis of the visual response in zebrafish larvae.Journal of visualized experiments : JoVE · 2015Article
- Defining the gene repertoire and spatiotemporal expression profiles of adhesion G protein-coupled receptors in zebrafish.BMC genomics · 2015Article
- Identification of amacrine subtypes that express the atypical cadherin celsr3.Experimental eye research · 2015Article
- Understanding cadherin EGF LAG seven-pass G-type receptors.Journal of neurochemistry · 2014Review
- Regulation of the protocadherin Celsr3 gene and its role in globus pallidus development and connectivity.Molecular and cellular biology · 2014Article
- Abnormal differentiation of dopaminergic neurons in zebrafish trpm7 mutant larvae impairs development of the motor pattern.Developmental biology · 2014Article
- Ionotropic GABA Receptors and Distal Retinal ON and OFF Responses.Scientifica · 2014Review
- Loss of Pde6 reduces cell body Ca(2+) transients within photoreceptors.Cell death & disease · 2013Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The identity of the specific molecules required for the process of retinal circuitry formation is largely unknown. Here we report a newly identified zebrafish mutant in which the absence of the atypical cadherin, Celsr3, leads to a specific defect in the development of GABAergic signaling in the inner retina. This mutant lacks an optokinetic response (OKR), the ability to visually track rotating illuminated stripes, and develops a super-normal b-wave in the electroretinogram (ERG). We find that celsr3 mRNA is abundant in the amacrine and ganglion cells of the retina, however its loss does not affect synaptic lamination within the inner plexiform layer (IPL) or amacrine cell number. We localize the ERG defect pharmacologically to a late-stage disruption in GABAergic modulation of ON-bipolar cell pathway and find that the DNQX-sensitive fast b1 component of the ERG is specifically affected in this mutant. Consistently, we find an increase in GABA receptors on mutant ON-bipolar terminals, providing a direct link between the observed physiological changes and alterations in GABA signaling components. Finally, using blastula transplantation, we show that the lack of an OKR is due, at least partially, to Celsr3-mediated defects within the brain. These findings support the previously postulated inner retina origin for the b1 component and reveal a new role for Celsr3 in the normal development of ON visual pathway circuitry in the inner retina.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.