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.

甲壳动物的 Y 器官分泌蜕皮激素。蜕皮激素在蜕皮前释放量增加，在血淋巴中循环，并刺激靶细胞中导致蜕皮的事件。在蜕皮周期的大部分时间里，蜕皮激素 (MIH) 会抑制蜕皮激素的产生，这是一种在眼柄中产生的肽神经激素。MIH 的抑制作用是由环核苷酸第二信使介导的。循环 MIH 的减少与蜕皮前血淋巴蜕皮激素滴度的增加有关。然而，长期以来一直假设积极的调节信号或刺激也参与促进蜕皮前蜕皮。^{这里审查的数据与细胞内 Ca 2+}的假设一致信号提供了这种刺激。增加 Y 器官细胞内 Ca ²⁺的药物促进蜕皮激素生成，而降低细胞内 Ca ²⁺或破坏 Ca ²⁺信号传导的药物抑制蜕皮激素生成。此外，眼柄消融后或自然预蜕皮期间血淋巴蜕皮激素滴度的增加与Y 器官细胞中细胞内游离 Ca ^{2+的增加有关。}几条证据表明，细胞内钙的升高与通过激活 Ca ^{2+增强的蜕皮激素生成有关}钙调素依赖性环核苷酸磷酸二酯酶，从而降低细胞内环核苷酸第二信使水平并促进蜕皮类固醇生成。转录组学研究的结果表明，参与 Ca ²⁺信号传导的基因在 Y 器官中得到了很好的体现。最近的几项研究集中在 Y 器官中的Ca ^{2+转运蛋白上。}已从蟹 Y 器官克隆了编码质膜 Ca ²⁺ ATP 酶 (PMCA) 和肌质/内质网 Ca ^{2+ ATP 酶 (SERCA) 的互补 DNA。}Y 器官中 PMCA 和 SERCA 转录物的相对丰度在蜕皮前升高，此时 Ca ²⁺Y 器官中的水平同样升高。结果与这些转运蛋白的作用是维持跨细胞膜的Ca ^{2+梯度并为未来的Ca 2+}信号重新设置细胞的概念是一致的。