Calcium signaling and regulation of ecdysteroidogenesis in crustacean Y-organs.

Autor: Weiner AC; Department of Biology, University of Alabama at Birmingham, Birmingham, AL 35294, United States., Chen HY; Department of Biology, University of Alabama at Birmingham, Birmingham, AL 35294, United States., Roegner ME; Department of Biology, University of Alabama at Birmingham, Birmingham, AL 35294, United States., Watson RD; Department of Biology, University of Alabama at Birmingham, Birmingham, AL 35294, United States. Electronic address: rdwatson@uab.edu.
Jazyk: angličtina
Zdroj: General and comparative endocrinology [Gen Comp Endocrinol] 2021 Dec 01; Vol. 314, pp. 113901. Date of Electronic Publication: 2021 Sep 14.
DOI: 10.1016/j.ygcen.2021.113901
Abstrakt: 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 2+ signal provides that stimulus. Pharmacological agents that increase intracellular Ca 2+ in Y-organs promote ecdysteroidogenesis, while agents that lower intracellular Ca 2+ or disrupt Ca 2+ 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 2+ in Y-organ cells. Several lines of evidence suggest elevated intracellular calcium is linked to enhanced ecdysteroidogenesis through activation of Ca 2+ /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 2+ signaling are well represented in Y-organs. Several recent studies have focused on Ca 2+ transport proteins in Y-organs. Complementary DNAs encoding a plasma membrane Ca 2+ ATPase (PMCA) and a sarcoplasmic/endoplasmic reticulum Ca 2+ 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 2+ levels in Y-organs are likewise elevated. The results are consistent with the notion that these transport proteins act to maintain the Ca 2+ gradient across the cell membrane and re-set the cell for future Ca 2+ signals.
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Databáze: MEDLINE