Antagonistic regulation by insulin-like peptide and activin ensures the elaboration of appropriate dendritic field sizes of amacrine neurons
Jiangnan Luo,
Chun-Yuan Ting,
Yan Li,
Philip McQueen,
Tzu-Yang Lin,
Chao-Ping Hsu,
Chi-Hon Lee
Affiliations
Jiangnan Luo
Section on Neuronal Connectivity, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, United States
Section on Neuronal Connectivity, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, United States
Yan Li
Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan, Republic of China
Philip McQueen
Mathematical and Statistical Computing Laboratory, Center for Information Technology, National Institutes of Health, Bethesda, United States
Tzu-Yang Lin
Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan, Republic of China
Chao-Ping Hsu
Institute of Chemistry, Academia Sinica, Taipei, Taiwan, Republic of China; Genome and Systems Biology Degree Program, National Taiwan University and Academia Sinica, Taipei, Taiwan, Republic of China
Section on Neuronal Connectivity, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, United States; Institute of Cellular and Organismic Biology, Academia Sinica, Taipei, Taiwan, Republic of China
Establishing appropriate sizes and shapes of dendritic arbors is critical for proper wiring of the central nervous system. Here we report that Insulin-like Peptide 2 (DILP2) locally activates transiently expressed insulin receptors in the central dendrites of Drosophila Dm8 amacrine neurons to positively regulate dendritic field elaboration. We found DILP2 was expressed in L5 lamina neurons, which have axonal terminals abutting Dm8 dendrites. Proper Dm8 dendrite morphogenesis and synapse formation required insulin signaling through TOR (target of rapamycin) and SREBP (sterol regulatory element-binding protein), acting in parallel with previously identified negative regulation by Activin signaling to provide robust control of Dm8 dendrite elaboration. A simulation of dendritic growth revealed trade-offs between dendritic field size and robustness when branching and terminating kinetic parameters were constant, but dynamic modulation of the parameters could mitigate these trade-offs. We suggest that antagonistic DILP2 and Activin signals from different afferents appropriately size Dm8 dendritic fields.
