859C Poster - 13. Neural development and physiology
Saturday April 09, 1:30 PM - 3:30 PM
Steroid hormone signaling activates a sensory switch during Drosophila peripheral nervous system development
Authors: Jacob Jaszczak 1,2; Laura DeVault 1,3; Lily Jan 1,2; Yuh-Nung Jan 1,2
Affiliations: 1) Department of Physiology, Department of Biochemistry and Biophysics, University of California at San Francisco, San Francisco, California, USA; 2) Howard Hughes Medical Institute; 3) Department of Developmental Biology, Washington University Medical School, Saint Louis, USA
Keywords: r. sensory cell development; c. hormones
Sensory neurons which detect multiple types of stimuli enable animals to sense environmental changes and avoid harm. How the neuronal properties which facilitate sensation are activated during development and the mechanisms which allow neurons to distinguish sensory modalities are poorly understood. The Class 4 dendritic arborization (C4da) neurons are multimodal sensors which tile the body wall of Drosophila larvae and detect temperature, light, and mechanical force. The development of the sensory responses mediated by C4da neurons demonstrates that the sensory function and modality are developmentally tuned processes. While larvae respond to mechanical force throughout development (Almeida-Carvalho et al. 2017), a robust activation of the thermal nociceptive escape behavior is only present during the second half of larval development (3rd instar) (Sulkowski et al. 2011). In contrast to the increase in nociceptive behavior in the 3rd instar, we find that ultraviolet light-induced Ca2+ activity in C4da neurons decreases during the same period of larval development. This demonstrates that different modalities detected by the same sensory neuron can each have different developmental patterns of activity. The steroid hormone receptor Ecdysone Receptor A (EcR.A) is required for thermal nociception in 3rd instar C4da neurons (McParland et al. 2015); thus, we examined the role of ecdysone in the sensory switch. We find that EcR nuclear localization increases early in the 3rd instar, and demonstrate that both increasing ecdysone titer and overexpression of EcR.A is sufficient to promote precocious thermal nociceptive responses in 2nd instar larvae. Additionally, we find that both 2nd instar and 3rd instar nociception requires EcR.A ligand dependent activation to promote thermal nociception. We next measured the expression of known nociceptive channels. While most of the channels have changing expression from 2nd to 3rd instar, we find EcR.A suppresses expression of subdued (encoding a TMEM16 channel) with indiscernible effect on the other nociceptive genes. RNAi reduction of subdued expression in 2nd instar C4da neurons not only increases thermal nociception, phenocopying EcR.A overexpression, but also decreases the response to ultraviolet light. Thus, steroid hormone signaling suppression of subdued expression facilitates the sensory switch of C4da neurons, and suggests that ion channel balance is a key target for tuning the development of sensory modalities.