Characterization of myoinhibitory peptide signaling system and its implication in larval metamorphosis and spawning behavior in Pacific abalone

•Abalone myoinhibitory peptides (Hdh-MIPs) act as ligands for the MIP receptor.•WX5-7Wamide motif in Hdh-MIPs is critical for Hdh-MIP signaling.•Hdh-MIP precursor and Hdh-MIPR are mainly expressed in the neural ganglia.•Hdh-MIPs inhibits larval metamorphosis but stimulates spawning behavior in abalo...

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Veröffentlicht in:General and comparative endocrinology 2024-07, Vol.353, p.114521, Article 114521
Hauptverfasser: Park, Sungwoo, Kim, Mi Ae, Sohn, Young Chang
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Sprache:eng
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Zusammenfassung:•Abalone myoinhibitory peptides (Hdh-MIPs) act as ligands for the MIP receptor.•WX5-7Wamide motif in Hdh-MIPs is critical for Hdh-MIP signaling.•Hdh-MIP precursor and Hdh-MIPR are mainly expressed in the neural ganglia.•Hdh-MIPs inhibits larval metamorphosis but stimulates spawning behavior in abalone. Myoinhibitory peptides (MIPs) affect various physiological functions, including juvenile hormone signaling, muscle contraction, larval development, and reproduction in invertebrates. Although MIPs are ligands for MIP and/or sex peptide receptors (MIP/SPRs) in diverse arthropods and model organisms belonging to Lophotrochozoa, the MIP signaling system has not yet been fully investigated in mollusks. In this study, we identified the MIP signaling system in the Pacific abalone Haliotis discus hannai (Hdh). Similar to the invertebrate MIPs, a total of eight paracopies of MIPs (named Hdh-MIP1 to Hdh-MIP8), harboring a WX5-7Wamide motif, except for Hdh-MIP2, were found in the Hdh-MIP precursor. Furthermore, we characterized a functional Hdh-MIPR, which responded to the Hdh-MIPs, except for Hdh-MIP2, possibly linked with the PKC/Ca2+ and PKA/cAMP signaling pathways. Hdh-MIPs delayed larval metamorphosis but increased the spawning behavior. These results suggest that the Hdh-MIP signaling system provides insights into the unique function of MIP in invertebrates.
ISSN:0016-6480
1095-6840
1095-6840
DOI:10.1016/j.ygcen.2024.114521