Interactions with presynaptic photoreceptors mediated by the Dpr11 and DIP-γ cell surface proteins control selection and survival of Drosophila amacrine neurons
Abstract
Drosophila R7 UV photoreceptors (PRs) are divided into yellow (y) and pale (p) subtypes with different wavelength sensitivities. yR7 PRs express the Dpr11 cell surface protein and are presynaptic to Dm8 amacrine neurons (yDm8) that express Dpr11's binding partner DIP-γ, while pR7 PRs synapse onto DIP-γ-negative pDm8 neurons. Dpr11 and DIP-γ expression patterns define yellow and pale medulla color vision circuits that project to higher-order areas. DIP- γ and dpr11 mutations affect the morphology of yDm8 arbors in the yellow circuit. yDm8 neurons are generated in excess during development and compete for presynaptic yR7 partners. Transsynaptic interactions between Dpr11 and DIP-γ are required for generation of neurotrophic signals that allow yDm8 neurons to survive. yDm8 and pDm8 neurons do not normally compete for neurotrophic support, but can be forced to do so by manipulating R7 subtype fates. DIP-γ-Dpr11 interactions allow yDm8 neurons to select yR7 PRs as their home column partners.
Additional Information
The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-NC-ND 4.0 International license. bioRxiv preprint first posted online Jun. 22, 2019. We thank Maximilien Courgeon and Claude Desplan for sharing unpublished antibodies and fly lines and for discussions, Larry Zipursky for sharing unpublished fly lines, comments on the manuscript and discussions, and Tim Mosca for his ExM protocol. We thank Violana Nesterova for figure preparation, Shuwa Xu for comments on the manuscript and discussions during the course of the work and Namrata Bali for help with ExM. The dpr11 RNAi stock was obtained from the Vienna Drosophila Resource Center (VDRC, www.vdrc.at). Stocks obtained from the Bloomington Drosophila Stock Center (NIHP40OD018537) were used in this study. Imaging was performed in the Biological Imaging Facility, with the support of the Caltech Beckman Institute and the Arnold and Mabel Beckman Foundation. Anti-Pros MR1A (mouse 1:4), anti-Elav 7E8A10 (rat, 1:10), anti-Dac 2-3 (mouse 1:50), anti-chaoptin 24B10 (mouse 1:20) were obtained from the Developmental Studies Hybridoma Bank (University of Iowa, IA). This work was supported by NIH grants RO1 EY028116 and R37 NS28182 to K. Z, and by the Howard Hughes Medical Institute (S-Y. T). Author contributions: Kaushiki P. Menon, Conceptualization, Supervision, Formal analysis, Validation, Investigation, Visualization, Methodology, Writing—original draft, Writing—review and editing; Vivek Kulkarni, Formal analysis, Validation, Investigation, Visualization, Methodology, Writing—review and editing; Shin-ya Takemura, Formal analysis, Validation, Investigation, Visualization, Writing—review and editing; Michael Anaya, Resources; Kai Zinn, Conceptualization, Supervision, Funding acquisition, Writing—original draft, Writing— review and editing, Project administration.Attached Files
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Additional details
- Eprint ID
- 96672
- Resolver ID
- CaltechAUTHORS:20190624-141606104
- NIH
- P40OD018537
- Caltech Beckman Institute
- Arnold and Mabel Beckman Foundation
- NIH
- RO1 EY028116
- NIH
- R37 NS28182
- Howard Hughes Medical Institute (HHMI)
- Created
-
2019-06-25Created from EPrint's datestamp field
- Updated
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2021-11-16Created from EPrint's last_modified field