Department of Biology, University of Alabama at Birmingham, Birmingham, AL 35294, United States.
Department of Biology, University of Alabama at Birmingham, Birmingham, AL 35294, United States.
Gen Comp Endocrinol. 2021 Dec 1;314:113901. doi: 10.1016/j.ygcen.2021.113901. Epub 2021 Sep 14.
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 Ca signal provides that stimulus. Pharmacological agents that increase intracellular Ca in Y-organs promote ecdysteroidogenesis, while agents that lower intracellular Ca or disrupt Ca 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 Ca in Y-organ cells. Several lines of evidence suggest elevated intracellular calcium is linked to enhanced ecdysteroidogenesis through activation of Ca/calmodulin dependent cyclic nucleotide phosphodiesterase, thereby lowering intracellular cyclic nucleotide second messenger levels and promoting ecdysteroidogenesis. Results of transcriptomic studies show genes involved in Ca signaling are well represented in Y-organs. Several recent studies have focused on Ca transport proteins in Y-organs. Complementary DNAs encoding a plasma membrane Ca ATPase (PMCA) and a sarcoplasmic/endoplasmic reticulum Ca 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 Ca levels in Y-organs are likewise elevated. The results are consistent with the notion that these transport proteins act to maintain the Ca gradient across the cell membrane and re-set the cell for future Ca signals.
甲壳类动物的 Y 器官分泌蜕皮激素。蜕皮激素在蜕皮前大量释放，在血淋巴中循环，并刺激靶细胞中的事件，导致蜕皮。在蜕皮周期的大部分时间里，蜕皮抑制激素 (MIH) 抑制蜕皮激素的产生，MIH 是一种在眼柄中产生的肽神经激素。MIH 的抑制作用是通过环核苷酸第二信使介导的。循环 MIH 的减少与蜕皮前血淋巴中蜕皮激素滴度的增加有关。然而，长期以来，人们一直假设在蜕皮前促进蜕皮激素生成也涉及到一个正调控信号或刺激物。这里回顾的数据与假设一致，即细胞内 Ca 信号提供了这种刺激。增加 Y 器官细胞内 Ca 的药理学制剂促进蜕皮激素生成，而降低细胞内 Ca 或破坏 Ca 信号的制剂则抑制蜕皮激素生成。此外，眼柄切除或自然蜕皮前血淋巴中蜕皮激素滴度的增加与 Y 器官细胞内游离 Ca 的增加有关。有几条证据表明，升高的细胞内钙通过激活 Ca/钙调蛋白依赖性环核苷酸磷酸二酯酶与增强的蜕皮激素生成有关，从而降低细胞内环核苷酸第二信使水平并促进蜕皮激素生成。转录组学研究的结果表明，参与 Ca 信号的基因在 Y 器官中得到了很好的表达。最近的几项研究集中在 Y 器官中的 Ca 转运蛋白上。从蟹类 Y 器官中克隆出质膜 Ca ATP 酶 (PMCA) 和肌浆/内质网 Ca ATP 酶 (SERCA) 的 cDNA。PMCA 和 SERCA 转录物在 Y 器官中的相对丰度在蜕皮前升高，此时 Y 器官中的 Ca 水平也升高。结果与这些转运蛋白作用是维持跨细胞膜的 Ca 梯度并为未来的 Ca 信号重置细胞的观点一致。
