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. 2017 Nov 22;6:e29797. doi: 10.7554/eLife.29797

Figure 7. ETHRB-expressing and non-CCAP/ETHRA neurons regulate Phase I.

Figure 7.

(A) Pupal CNS wholemount showing the expression pattern of ETHRB-Gal4 (green, UAS-6XGFP). VNC, ventral nerve cord. Scale bar: 50 µm. (B) Similar to (A), but showing the expression pattern of ETHRA-Gal4 excluding the neurons that express CCAP. Gal4 activity in the latter neurons was blocked using CCAP-Gal80. Scale bar: 50 µm. (C–D) Behavioral effects of suppressing either: (C) ETHRB-expressing neurons, or (D) non-CCAP/ETHRA neurons. Unlike unsuppressed control animals (upper graphs), animals in which ETHRB-expressing neurons are suppressed (C, bottom) lack Phase I, and this phase is significantly shortened (p-0.014) by suppression of non-ETHRA/CCAP neurons (D, bottom). Bar graphs show average phase durations ± standard deviations, (N in parentheses). (E) Hierarchical organization of the pupal ecdysis circuit. Each layer in the network hierarchy (red) is the target of one of the ecdysis hormones (blue), as defined by expression of its receptor. The most important component of the input layer, ETHRA/CCAP, participates in regulating all three behavioral phases and is the source of CCAP and Bursicon. Bursicon’s receptor, Rk, defines a central pattern generating layer, which sends output to a population of motor neurons that express the receptor for CCAP and are required for the ecdysis sequence. Solid arrows indicate demonstrated functional connections, while gray, dashed arrows indicate hypothesized connections. Although the detailed mechanisms governing motor program progression remain to be determined, those that promote Phase II negatively regulate Phase I and positively regulate Phase III.