Abstract
Neuropeptides, as pervasive intercellular signaling molecules in the CNS, modulate a variety of behavioral systems in both protostomes and deuterostomes. Allatostatins are neuropeptides in arthropods that inhibit the biosynthesis of juvenile hormones. Based on amino acid sequences, they are divided into three different types in arthropods: allatostatin A, allatostatin B, allatostatin C. Allatostatin C (AstC) was first isolated from Manduca sexta, and it has an important conserved feature of a disulfide bridge formed by two cysteine residues. Moreover, AstC appears to be the ortholog of mammalian somatostatin, and it has functions in common with somatostatin, such as modulating feeding behaviors. The AstC signaling system has been widely studied in arthropods, but minimally studied in molluscs. In this study, we seek to identify the AstC signaling system in the marine mollusc Aplysia californica. We cloned the AstC precursor from the cDNA of Aplysia. We predicted a 15-amino acid peptide with a disulfide bridge, i.e., AstC, using NeuroPred. We then cloned two putative allatostatin C-like receptors and through NCBI Conserved Domain Search we found that they belonged to the G protein-coupled receptor (GPCR) family. In addition, using an inositol monophosphate 1 (IP1) accumulation assay, we showed that Aplysia AstC could activate one of the putative receptors, i.e., the AstC-R, at the lowest EC50, and AstC without the disulfide bridge (AstC') activated AstC-R with the highest EC50. Moreover, four molluscan AstCs with variations of sequences from Aplysia AstC but with the disulfide bridge activated AstC-R at intermediate EC50. In summary, our successful identification of the Aplysia AstC precursor and its receptor (AstC-R) represents the first example in molluscs, and provides an important basis for further studies of the AstC signaling system in Aplysia and other molluscs.
Original language | English |
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Article number | 1213 |
Journal | Scientific Reports |
Volume | 12 |
Issue number | 1 |
Early online date | 24 Jan 2022 |
DOIs | |
State | Published - 24 Jan 2022 |
Bibliographical note
Publisher Copyright:© 2022, The Author(s).
Funding
We thank the two anonymous reviewers for their useful comments that we used to improve our manuscript. This work was supported by the National Natural Science Foundation of China (Grant 31861143036, 62050071, 32171011, 32100816, 31671097, 31371104), Jiangsu Science and Technology Department Grant BK20210183 and Israel Science Foundation Grant 2396/18. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Funders | Funder number |
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National Natural Science Foundation of China | 31861143036, 31371104, 32100816, 62050071, 32171011, 31671097 |
Israel Science Foundation | 2396/18 |
Jiangsu Science and Technology Department | BK20210183 |