Alami Meriem, Vacher Hélène, Bosmans Frank, Devaux Christiane, Rosso Jean-Pierre, Bougis Pierre E, Tytgat Jan, Darbon Hervé, Martin-Eauclaire Marie-France
CNRS UMR 6560, Ingénierie des Protéines, Faculté de Médecine secteur Nord, Institut Jean Roche, Université de la Méditerranée, Bd Pierre Dramard, 13916, Marseille, Cedex 20, France.
Biochem J. 2003 Nov 1;375(Pt 3):551-60. doi: 10.1042/BJ20030688.
The venom of the scorpion Androctonus mauretanicus mauretanicus was screened by use of a specific serum directed against AaH II, the scorpion alpha-toxin of reference, with the aim of identifying new analogues. This led to the isolation of Amm VIII (7382.57 Da), which gave a highly positive response in ELISA, but was totally devoid of toxicity when injected subcutaneously into mice. In voltage-clamp experiments with rat brain type II Na+ channel rNa(v)1.2 or rat skeletal muscle Na+ channel rNa(v)1.4, expressed in Xenopus oocytes, the EC50 values of the toxin-induced slowing of inactivation were: 29+/-5 and 416+/-14 nM respectively for AmmVIII and 2.6+/-0.3 nM and 2.2+/-0.2 nM, respectively, for AaH II interactions. Accordingly, Amm VIII clearly discriminates neuronal versus muscular Na+ channel. The Amm VIII cDNA was amplified from a venom gland cDNA library and its oligonucleotide sequence determined. It shows 87% sequence homology with AaH II, but carries an unusual extension at its C-terminal end, consisting of an additional Asp due to a point mutation in the cDNA penultimate codon. We hypothesized that this extra amino acid residue could induce steric hindrance and dramatically reduce recognition of the target by Amm VIII. We constructed a model of Amm VIII based on the X-ray structure of AaH II to clarify this point. Molecular modelling showed that this C-terminal extension does not lead to an overall conformational change in Amm VIII, but drastically modifies the charge repartition and, consequently, the electrostatic dipole moment of the molecule. At last, liquid-phase radioimmunassays with poly- and monoclonal anti-(AaH II) antibodies showed the loss of conformational epitopes between AaH II and Amm VIII.
使用针对AaH II(参考蝎α毒素)的特异性血清对毛里塔尼亚杀人蝎毒液进行筛选,旨在鉴定新的类似物。这导致分离出Amm VIII(7382.57道尔顿),其在酶联免疫吸附测定(ELISA)中给出高度阳性反应,但皮下注射到小鼠体内时完全没有毒性。在用非洲爪蟾卵母细胞中表达的大鼠脑II型Na⁺通道rNa(v)1.2或大鼠骨骼肌Na⁺通道rNa(v)1.4进行的电压钳实验中,毒素诱导失活减慢的半数有效浓度(EC50)值分别为:Amm VIII为29±5和416±14 nM,AaH II相互作用时分别为2.6±0.3 nM和2.2±0.2 nM。因此,Amm VIII能清晰区分神经元型与肌肉型Na⁺通道。从毒液腺cDNA文库中扩增出Amm VIII cDNA并确定其寡核苷酸序列。它与AaH II的序列同源性为87%,但在其C末端有一个不寻常的延伸,由于cDNA倒数第二个密码子中的点突变导致额外有一个天冬氨酸。我们推测这个额外的氨基酸残基可能会引起空间位阻,并显著降低Amm VIII对靶标的识别。我们基于AaH II的X射线结构构建了Amm VIII模型以阐明这一点。分子模拟表明,这个C末端延伸不会导致Amm VIII整体构象变化,但会极大地改变电荷分布,从而改变分子的静电偶极矩。最后,用多克隆和单克隆抗(AaH II)抗体进行的液相放射免疫测定显示AaH II和Amm VIII之间构象表位的丧失。