Biggers W J, Laufer H
Biol Bull. 1999 Apr;196(2):187-198. doi: 10.2307/1542564.
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 RIM-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 KCI. 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 Ni2+, Zn2+, 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.
研究了保幼激素活性化合物诱导多毛纲环节动物小头虫（Capitella sp. 1）后担轮幼虫沉降和变态的信号转导途径。已知的蛋白激酶C（PKC）激活剂佛波醇-12,13-二丁酸酯是沉降和变态的活性诱导剂，而PKC抑制剂H-7抑制了对保幼激素III（JH III）的沉降和变态反应。JH III和法尼酸甲酯（MF）在体外也直接激活了小头虫匀浆中存在的一种PKC样酶以及从大鼠脑中纯化的PKC。此外，使用荧光PKC抑制剂RIM-1的结合研究揭示了完整的小头虫幼虫和幼体中存在一种PKC样酶。幼虫的沉降和变态也受到膜去极化浓度的氯化钾的刺激。这种对氯化钾的反应被四乙铵抑制。钾通道阻滞剂4-氨基吡啶诱导沉降和变态，而对JH III的沉降和变态反应被钾通道离子载体尼日利亚菌素抑制。JH III诱导的沉降和变态被钙通道阻滞剂Ni2+、Zn2+和维拉帕米抑制，而钙离子载体A23187诱导沉降和变态。这些结果表明，在介导这种反应时，保幼激素可能会导致PKC的激活，从而导致随后钾通道和钙通道的调节。
