Meeting Abstract
Growth in decapod crustaceans occurs by the shedding of the exoskeleton in a process known as molting. The molt cycle is comprised of three stages; intermolt, premolt and postmolt. The premolt stage is further broken down into three phases, early, mid and late, which are defined by changes in molting hormone titers in the hemolymph. Molting hormones, or ecdysteroids, are synthesized and released from the molting gland, the Y-organ (YO). Ecdysteroid synthesis is regulated by a neuropeptide, molt inhibiting hormone (MIH), which binds a receptor on the surface of the YO and represses ecdysteroidgenesis. MIH is synthesized in the X-organ (XO) and secreted from the sinus gland (SG) of the eyestalk ganglia (ESG). Removal of the ESG via eyestalk ablation (ESA) eliminates the primary source of MIH, stimulating ecdysteroid synthesis by the YO. The proposed MIH signaling pathway involves a cAMP/Ca2+-dependent triggering phase, followed by NO synthase (NOS)/cGMP-dependent summation phase. Analysis of a YO baseline transcriptome identified the components of the MIH pathway: adenylyl cyclase (AC), calmodulin (CaM), calcineurin (CaN), NOS, NOS inhibitory protein (NOSIP), NO-sensitive guanylyl cyclase (GC-I), protein kinase G (PKG), and the catalytic β -subunit of protein kinase A (PKA). ESA increased Gl-NOS and Gl-GC-I mRNA levels in the YO, but the effects of ESA on the other signaling components was not determined. These data suggest that the YO responses to acute MIH withdrawal by increasing its sensitivity to MIH. Quantitative PCR is being used to determine the effects of ESA on the expression of Gl-AC, Gl-CaM, Gl-CaN, Gl-NOS, Gl-NOSIP, Gl-GC-I, Gl-PKA, and Gl-PKG in the YO. Supported by NSF (IOS-1257732).
