[Hyp3]Met-callatostatin. Identification and biological properties of a novel neuropeptide from the blowfly Calliphora vomitoria.
[Hyp3]Met-callatostatin. Identification and biological properties of a novel neuropeptide from the blowfly Calliphora vomitoria.
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[Hyp3]Met-callatostatin。
DOI：
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发表时间：
1994
影响因子：
4.8
通讯作者：
A. Thorpe
中科院分区：
文献类型：
--
作者：
H. Duve;A. Johnsen;A. G. Scott;P. East;A. Thorpe
从呕吐丽蝇（Calliphora vomitoria）头部提取物中鉴定出一种新的含羟脯氨酸的神经肽，命名为[HYP 3] Met-卡拉图他汀（callatostatin）。该肽是一种天然存在的羟基化类似物的Met-callatostatin，以前确定的allatostatin样肽，并存在的程度为20%的非羟基化形式。在生物测定中，两种形式的肽通过抑制蟑螂美洲大蠊、斑点双翅虫和德国小蠊中的保幼激素合成和释放而显示出抑异生长活性（IC 50 = 100 pM-10 nM）。然而，它们不影响青头苍蝇中保幼激素bisepoxide的合成和释放。在果蝇中，[Hyp 3] Met-卡拉图他汀抑制后肠的蠕动运动，与Met-卡拉图他汀的双相反应（IC 50 = 100 nM）相比，显示出双相反应（IC 50 = 0.5 pM和0.5 μ M）。免疫细胞化学研究Met-卡拉图他汀抗血清提供了在肠道中的肌抑制作用的细胞学基础，因为在腹部神经节中的免疫反应性神经元的轴突投射到回肠。在中肠中也有内分泌细胞，通过将肽释放到血淋巴中，将允许Met-卡拉他汀在肠道和心脏的肌肉上发挥神经激素作用。相比之下，从大脑到产生保幼激素的腺体--咽侧体，没有Met-卡拉图他汀神经通路。与美洲大蠊血淋巴一起孵育的Met-卡拉他汀的NH 2-末端降解导致Pro-Tyr键的裂解，得到五肽Tyr-Asp-Phe-Gly-Met-NH 2作为降解产物。相反，Hyp-Tyr键抵抗裂解。用C.呕吐，没有免疫测定的降解产物已观察到与任何肽。
A novel, hydroxyproline-containing neuropeptide, Gly-Pro-Hyp-Tyr-Asp-Phe-Gly-Met-NH2, designated [HYP3]Met-callatostatin, has been identified from extracts of heads of the blowfly Calliphora vomitoria. The peptide is a naturally occurring hydroxylate analogue of Met-callatostatin, a previously identified allatostatin-like peptide, and is present to the extent of 20% of the nonhydroxylated form. In bioassays, both forms of the peptide show allatostatic activity by inhibiting juvenile hormone synthesis and release in the cockroaches Periplaneta americana, Diploptera punctata, and Blattella germanica (IC50 = 100 pM-10 nM). They do not, however, influence juvenile hormone bisepoxide synthesis and release in the blowfly. In flies, [Hyp3]Met-callatostatin inhibits the peristaltic movements of the hindgut, showing a biphasic response (IC50 = 0.5 pM and 0.5 microM) compared with the monophasic response of Met-callatostatin (IC50 = 100 nM). Immunocytochemical studies with Met-callatostatin antisera provide the cytological basis for a myoinhibitory role in the gut since the axons of immunoreactive neurons in the abdominal ganglion project to the ileum. There are also endocrine cells in the midgut that, by releasing the peptides into the hemolymph, would allow the Met-callatostatins to fulfill a neurohormonal role on muscles of the gut and heart. In contrast, there are no Met-callatostatin neural pathways from the brain to the corpus allatum, the gland that produces juvenile hormone. NH2-terminal degradation of Met-callatostatins incubated with the hemolymph of P. americana results in cleavage of the Pro-Tyr bond giving the pentapeptide Tyr-Asp-Phe-Gly-Met-NH2 as a degradation product. In contrast, the Hyp-Tyr bond resists cleavage. With hemolymph from C. vomitoria, no immunoassayable degradation product has been observed with either peptide.