Calcium signaling and regulation of ecdysteroidogenesis in crustacean Y-organs

Crustacean Y-organs secrete ecdysteroid molting hormones. Ecdysteroids are released in increased amount during premolt, circulate in hemolymph, and stimulate the events in target cells that lead to molting. During much of the molting cycle, ecdysteroid production is suppressed by molt-inhibiting hormone (MIH), a peptide neurohormone produced in the eyestalks. The suppressive effect of MIH is mediated by a cyclic nucleotide second messenger. A decrease in circulating MIH is associated with an increase in the hemolymphatic ecdysteroid titer during pre-molt. Nevertheless, it has long been hypothesized that a positive regulatory signal or stimulus is also involved in promoting ecdysteroidogenensis during premolt. Data reviewed here are consistent with the hypothesis that an intracellular Ca²⁺ signal provides that stimulus. Pharmacological agents that increase intracellular Ca²⁺ in Y-organs promote ecdysteroidogenesis, while agents that lower intracellular Ca²⁺ or disrupt Ca²⁺ signaling suppress ecdysteroidogenesis. Further, an increase in the hemolymphatic ecdysteroid titer after eyestalk ablation or during natural premolt is associated with an increase in intracellular free Ca²⁺ in Y-organ cells. Several lines of evidence suggest elevated intracellular calcium is linked to enhanced ecdysteroidogenesis through activation of Ca²⁺/calmodulin dependent cyclic nucleotide phosphodiesterase, thereby lowering intracellular cyclic nucleotide second messenger levels and promoting ecdysteroidogenesis. Results of transcriptomic studies show genes involved in Ca²⁺ signaling are well represented in Y-organs. Several recent studies have focused on Ca²⁺ transport proteins in Y-organs. Complementary DNAs encoding a plasma membrane Ca²⁺ ATPase (PMCA) and a sarcoplasmic/endoplasmic reticulum Ca²⁺ ATPase (SERCA) have been cloned from crab Y-organs. The relative abundance of PMCA and SERCA transcripts in Y-organs is elevated during premolt, a time when Ca²⁺ levels in Y-organs are likewise elevated. The results are consistent with the notion that these transport proteins act to maintain the Ca²⁺ gradient across the cell membrane and re-set the cell for future Ca²⁺ signals.