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首页> 外文期刊>The Biological Bulletin >Settlement and Metamorphosis of Capitella Larvae Induced by Juvenile Hormone-Active Compounds Is Mediated by Protein Kinase C and Ion Channels
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Settlement and Metamorphosis of Capitella Larvae Induced by Juvenile Hormone-Active Compounds Is Mediated by Protein Kinase C and Ion Channels

机译:蛋白激酶C和离子通道介导幼体激素活性化合物诱导的小头虫幼虫的沉降和变态

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摘要

The signal transduction pathway by which juvenile hormone-active compounds induce settlement and metamorphosis of metatrochophore larvae of the polychaete annelid Capitella sp. 1 was investigated. The known protein kinase C (PKC) activator phorbol-12,13-dibutyrate was an active inducer of settlement and metamorphosis, whereas H-7, an inhibitor of PKC, inhibited settlement and metamorphosis in response to juvenile hormone III (JH III). JH III and methyl farnesoate (MF) also directly activated, in vitro, both a PKC-like enzyme present in Capitella homogenates and PKC purified from rat brain. In addition, binding studies using the fluorescent PKC inhibitor PIM-1 revealed the presence of a PKC-like enzyme in intact Capitella larvae and juveniles. Settlement and metamorphosis of the larvae was also stimulated by membrane-depolarizing concentrations of KC1. This response to KCl was inhibited by tetraethylammonium. The potassium channel blocker 4-aminopyridine induced settlement and metamorphosis, whereas settlement and metamorphosis in response to JH III was inhibited by the potassium channel ionophore nigericin. Settlement and metamorphosis induced by JH III was inhibited by the calcium channel blockers Ni~(2+), Zn~(2+), and verapamil, whereas settlement and metamorphosis was induced by the calcium ionophore A23187. These results suggest that in mediating this response, juvenile hormones may cause activation of PKC, leading to subsequent modulation of potassium and calcium channels.
机译:幼年激素活性化合物诱导多毛小an鱼Capitella sp。的变质回生幼虫沉降和变态的信号转导途径。 1被调查。已知的蛋白激酶C(PKC)激活物phorbol-12,13-dibutyrate是活性的沉降和变态诱导剂,而PKC的抑制剂H-7则响应少年激素III(JH III)抑制沉降和变态。 JH III和法呢酸甲酯(MF)在体外也直接激活了Capitella匀浆中存在的PKC样酶和从大鼠脑中纯化的PKC。此外,使用荧光PKC抑制剂PIM-1进行的结合研究表明,完整的小肠小肠幼虫和幼虫中存在PKC样酶。膜去极化浓度的KC1也刺激幼虫的沉降和变态。四乙基铵抑制了对KCl的反应。钾通道阻滞剂4-氨基吡啶诱导了沉降和变态,而钾通道离子载体尼日菌素抑制了对JH III的沉降和变态。钙离子通道阻滞剂Ni〜(2 +),Zn〜(2+)和维拉帕米抑制JH III诱导的沉降和变态,而钙离子载体A23187诱导沉降和变态。这些结果表明,在调解这种反应中,少年激素可能会导致PKC激活,从而导致钾和钙通道的后续调节。

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