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Characterization of a Receptor for Insect Tachykinin‐Like Peptide Agonists by Functional Expression in a Stable Drosophila Schneider 2 Cell Line
Author(s) -
Torfs Herbert,
Shariatmadari Ramin,
Guerrero Felix,
Parmentier Marc,
Poels Jeroen,
Van Poyer Wendy,
Swinnen Elfriede,
De Loof Arnold,
Åkerman Karl,
Vanden Broeck Jozef
Publication year - 2000
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.2000.0742182.x
Subject(s) - tachykinin receptor , biology , neurokinin a , receptor , pertussis toxin , microbiology and biotechnology , phospholipase c , substance p , inositol trisphosphate , second messenger system , inositol , calcium in biology , transfection , agonist , inositol phosphate , drosophila melanogaster , calcium , neurokinin b , neuropeptide , signal transduction , g protein , cell culture , medicine , biochemistry , genetics , gene
STKR is an insect G protein‐coupled receptor, cloned from the stable fly Stomoxys calcitrans . It displays sequence similarity to vertebrate tachykinin [or neurokinin (NK)] receptors. Functional expression of the cloned STKR cDNA was obtained in cultured Drosophila melanogaster Schneider 2 (S2) cells. Insect tachykinin‐like peptides or “insectatachykinins,” such as Locusta tachykinin ( Lom ‐TK) III, produced dose‐dependent calcium responses in stably transfected S2‐STKR cells. Vertebrate tachykinins (or neurokinins) did not evoke any effect at concentrations up to 10 ‐5 M , but an antagonist of mammalian neurokinin receptors, spantide II, inhibited the Lom ‐TK III‐induced calcium response. Further analysis showed that the agonist‐induced intracellular release of calcium ions was not affected by pretreatment of the cells with pertussis toxin. The calcium rise was blocked by the phospholipase C inhibitor U73122. In addition, Lom ‐TK III was shown to have a stimulatory effect on the accumulation of both inositol 1,4,5‐trisphosphate and cyclic AMP. These are the same second messengers that are induced in mammalian neurokinin‐dependent signaling processes.