Meeting Abstract

15.5  Wednesday, Jan. 4  Signaling pathways controlling the crustacean molting gland MYKLES, D.L.; Colorado State University, Fort Collins

Molting in decapod crustaceans is controlled by molt-inhibiting hormone (MIH), a neuropeptide that suppresses production of molting hormone (ecdysteroids) by a pair of molting glands (Y-organs or YOs). MIH signaling is organized into a cAMP/Ca2+-dependent “triggering” phase and a NO/cGMP-dependent “summation” phase linked by calmodulin. Molting can be induced by eyestalk ablation (ESA) or by multiple leg autotomy (MLA). During the molt cycle, the YO transitions through four physiological states, which are mediated by endocrine and autocrine/paracrine factors: “basal” state at postmolt and intermolt stages; “activated” state at early premolt; “committed” state at mid premolt; and “repressed” state at late premolt. The basal to activated state transition is triggered by a transient reduction in MIH; the YOs hypertrophy, but remain sensitive to MIH, as premolt is suspended by MIH injection or by limb bud autotomy (LBA). metazoan Target of Rapamycin (mTOR), which controls global translation of mRNA into protein, appears to be involved in YO activation in early premolt. At the activated to committed state transition, the animal becomes committed to molt, as the YO is less sensitive to MIH and premolt is not suspended by LBA. YO commitment involves a putative TGFβ factor, as SB431542, a TGFβ receptor antagonist, lowers hemolymph ecdysteroid titers in mid premolt animals. At the committed to repressed state transition, high 20-hydroxyecdysone levels inhibit YO ecdysteroid secretion and hemolymph titers fall. Molting, or ecdysis, marks the transition from the repressed to the basal state, during which the YO atrophies and regains sensitivity to MIH. A biosystems approach is proposed to define the role and interactions between the MIH, mTOR, and TGFβ signaling pathways at the transcriptional and posttranscriptional levels. Supported by NSF (IOS-0745224).