Institute of Microbiology of the CAS, v.v.i., Videnska 1083, 142 20, Prague, Czech Republic.
Charles University, Department of Genetics and Microbiology, Faculty of Science, Vinicna 5, 128 43, Prague, Czech Republic.
Sci Rep. 2019 Apr 8;9(1):5758. doi: 10.1038/s41598-019-42200-2.
The adenylate cyclase toxin-hemolysin (CyaA, ACT or AC-Hly) of pathogenic Bordetellae delivers its adenylyl cyclase (AC) enzyme domain into the cytosol of host cells and catalyzes uncontrolled conversion of cellular ATP to cAMP. In parallel, the toxin forms small cation-selective pores that permeabilize target cell membrane and account for the hemolytic activity of CyaA on erythrocytes. The pore-forming domain of CyaA is predicted to consist of five transmembrane α-helices, of which the helices I, III, IV and V have previously been characterized. We examined here the α-helix II that is predicted to form between residues 529 to 549. Substitution of the glycine 531 residue by a proline selectively reduced the hemolytic capacity but did not affect the AC translocating activity of the CyaA-G531P toxin. In contrast, CyaA toxins with alanine 538 or 546 replaced by diverse residues were selectively impaired in the capacity to translocate the AC domain across cell membrane but remained fully hemolytic. Such toxins, however, formed pores in planar asolectin bilayer membranes with a very low frequency and with at least two different conducting states. The helix-breaking substitution of alanine 538 by a proline residue abolished the voltage-activated increase of membrane activity of CyaA in asolectin bilayers. These results reveal that the predicted α-helix comprising the residues 529 to 549 plays a key role in CyaA penetration into the target plasma membrane and pore-forming activity of the toxin.
致病伯氏菌的腺苷酸环化酶毒素-溶血素 (CyaA、ACT 或 AC-Hly) 将其腺苷酸环化酶 (AC) 酶结构域递送到宿主细胞的细胞质中,并催化细胞内 ATP 的不受控制转化为 cAMP。同时,毒素形成小的阳离子选择性孔,使靶细胞膜通透性增加,这是 CyaA 对红细胞产生溶血活性的原因。CyaA 的孔形成结构域预计由五个跨膜α-螺旋组成,其中螺旋 I、III、IV 和 V 以前已被表征。我们在此研究了预测在残基 529 到 549 之间形成的α-螺旋 II。甘氨酸 531 残基被脯氨酸取代选择性降低了溶血能力,但不影响 CyaA-G531P 毒素的 AC 易位活性。相比之下,用多种残基取代丙氨酸 538 或 546 的 CyaA 毒素在跨细胞膜易位 AC 结构域的能力上受到选择性损害,但仍保持完全溶血活性。然而,这些毒素在平面大豆卵磷脂双层膜中形成孔的频率非常低,并且具有至少两种不同的导通状态。用脯氨酸残基取代丙氨酸 538 会破坏 CyaA 在大豆卵磷脂双层膜中的电压激活增加膜活性。这些结果表明,预测的由残基 529 到 549 组成的α-螺旋在 CyaA 穿透靶质膜和毒素的孔形成活性中发挥关键作用。