Meeting Abstract
Molting is controlled by ecdysteroids synthesized and secreted by the molting gland, or Y-organ (YO). Halloween genes encode enzymes that catalyze the synthesis of ecdysteroid hormones. Ecdysteroid receptor (EcR/RXR) binds active molting hormone, which induces serial activation of ecdysteroid-responsive genes. During premolt, TGFβ/activin signaling mediates the transition of the YO from the activated to the committed state, as SB431542 blocks this transition. G. lateralis were eyestalk-ablated to induce molting and injected with vehicle (DMSO) or SB431542 at Day 0. In controls, ESA increased hemolymph ecdysteroid titers at 3, 7 and 14 days post-ESA. There were significant increases in the mRNA levels of Gl-Nvd at 7 and 14 days post-ESA and other Halloween genes (Gl-Spo, Gl-Phm, Gl-Dib,Gl-Sad), as well as Gl-CYP18a1, Gl-ALAS, Gl-NADK, Gl-BR-C, Gl-EcR, and Gl-RXR, at 14 days post-ESA. SB431542 reduced hemolymph ecdysteroid titers at 7 and 14 days post-ESA compared to control animals, but titers were no different from controls at 1, 3, and 5 days post-ESA, indicating that SB431542 had no effect on YO activation. SB431542 blocked the increases in RNA levels of Gl-Nvd, Gl-Spo, Gl-Phm,Gl-Dib,Gl-Sad, Gl-CYP18a1,Gl-ALAS, Gl-NADK,Gl-BR-C,Gl-EcR,and Gl-RXR by ESA. SB431542 had no effect on mRNA levels of the ecdysteroid-responsive genes Gl-HR3, Gl-HR4,Gl-E74,Gl-E75 and Gl-FTZ-F1. These data suggest that an activin-like TGFβ factor stimulates YO ecdysteroidogenesis in the committed YO by up-regulating Halloween genes and the Gl-BR-C ecdysteroid-responsive gene. Supported by NSF (IOS-1257732).