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Published November 6, 2019 | Supplemental Material + Published
Journal Article Open

Interactions between Dpr11 and DIP-γ control selection of amacrine neurons in Drosophila color vision circuits


Drosophila R7 UV photoreceptors (PRs) are divided into yellow (y) and pale (p) subtypes. 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. Dpr11 and DIP-γ expression patterns define 'yellow' and 'pale' color vision circuits. We examined Dm8 neurons in these circuits by electron microscopic reconstruction and expansion microscopy. DIP-γ and dpr11 mutations affect the morphologies of yDm8 distal ('home column') dendrites. yDm8 neurons are generated in excess during development and compete for presynaptic yR7 PRs, and interactions between Dpr11 and DIP-γ are required for yDm8 survival. These interactions also allow yDm8 neurons to select yR7 PRs as their appropriate home column partners. yDm8 and pDm8 neurons do not normally compete for survival signals or R7 partners, but can be forced to do so by manipulation of R7 subtype fate.

Additional Information

© 2019 eLife Sciences Publications Ltd. Subject to a Creative Commons Attribution license, except where otherwise noted. Data availability: All data generated or analysed during this study are included in the manuscript and supporting files. We thank Larry Zipursky, Aljoscha Nern, Takashi Suzuki, and Michael Reiser for fly lines and discussions, Maximilien Courgeon and Claude Desplan for sharing unpublished antibodies and fly lines and for discussions, and Tim Mosca for his ExM protocol. We thank Violana Nesterova for figure preparation, Shuwa Xu and Larry Zipursky for comments on the manuscript, Shuwa Xu for 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 per- formed 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 KZ, and by the Howard Hughes Medical Institute (S-YT). The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication. Author contributions: Kaushiki P Menon, Conceptualization, Formal analysis, Supervision, 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, Investigation, Methodology; Kai Zinn, Conceptualization, Supervision, Funding acquisition, Writing—original draft, Project administration, Writing—review and editing.

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Published - elife-48935-v2.pdf

Supplemental Material - elife-48935-supp-v1.zip


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August 19, 2023
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