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  Adhesion GPCR Latrophilin 3 regulates synaptic function of cone photoreceptors in a trans-synaptic manner

Wang, Y., Cao, Y., Hays, C. L., Laboute, T., Ray, T. A., Guerrero-Given, D., et al. (2021). Adhesion GPCR Latrophilin 3 regulates synaptic function of cone photoreceptors in a trans-synaptic manner. Proceedings of the National Academy of Sciences, (45). Retrieved from https://www.pnas.org/content/118/45/e2106694118.

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Item Permalink: https://hdl.handle.net/21.11116/0000-000C-DFBE-4 Version Permalink: https://hdl.handle.net/21.11116/0000-000C-DFBF-3
Genre: Journal Article
Alternative Title : Proceedings of the National Academy of Sciences

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 Creators:
Wang, Yuchen, Author
Cao, Yan, Author
Hays, Cassandra L., Author
Laboute, Thibaut, Author
Ray, Thomas A., Author
Guerrero-Given, Debbie1, Author
Ahuja, Abhimanyu S., Author
Patil, Dipak, Author
Rivero, Olga, Author
Kamasawa, Naomi1, Author
Kay, Jeremy N., Author
Thoreson, Wallace B., Author
Martemyanov, Kirill A., Author
Affiliations:
1Max Planck Florida Institute for Neuroscience, Max Planck Society, One Max Planck Way, Jupiter FL 33458, USA, ou_1950288              

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Free keywords: adhesion GPCR, horizontal cells, retina, synapses, vision
 Abstract: Cone photoreceptors mediate daylight vision in vertebrates. Changes in neurotransmitter release at cone synapses encode visual information and is subject to precise control by negative feedback from enigmatic horizontal cells. However, the mechanisms that orchestrate this modulation are poorly understood due to a virtually unknown landscape of molecular players. Here, we report a molecular player operating selectively at cone synapses that modulates effects of horizontal cells on synaptic release. Using an unbiased proteomic screen, we identified an adhesion GPCR Latrophilin3 (LPHN3) in horizontal cell dendrites that engages in transsynaptic control of cones. We detected and characterized a prominent splice isoform of LPHN3 that excludes a element with inhibitory influence on transsynaptic interactions. A gain-of-function mouse model specifically routing LPHN3 splicing to this isoform but not knockout of LPHN3 diminished CaV1.4 calcium channel activity profoundly disrupted synaptic release by cones and resulted in synaptic transmission deficits. These findings offer molecular insight into horizontal cell modulation on cone synaptic function and more broadly demonstrate the importance of alternative splicing in adhesion GPCRs for their physiological function.

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 Dates: 2021
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: URI: https://www.pnas.org/content/118/45/e2106694118
URI: https://www.pnas.org/doi/pdf/10.1073/pnas.2106694118
URI: http://www.ncbi.nlm.nih.gov/pubmed/34732574
URI: https://www.pnas.org/content/118/45/e2106694118
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Title: Proceedings of the National Academy of Sciences
  Alternative Title : PNAS
Source Genre: Journal
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Publ. Info: -
Pages: - Volume / Issue: (45) Sequence Number: - Start / End Page: - Identifier: ISBN: 0027-8424, 1091-6490