Friedman E, Farfel Z, Hanski E
Biochem J. 1987 Apr 1;243(1):145-51. doi: 10.1042/bj2430145.
Bordetella pertussis, the causative organism of whooping cough, produces a calmodulin-sensitive adenylate cyclase. Confer & Eaton [(1982) Science 217, 948-950] have shown that an extract from B. pertussis increases intracellular cyclic AMP levels in neutrophils and suggested that this increase is caused by the bacterial adenylate cyclase which penetrates these cells. We demonstrate in the present study that adenylate cyclase activity in lysates from lymphocytes exposed to a partially purified preparation of the bacterial enzyme has properties completely different from those of the intrinsic membrane-bound enzyme. Adenylate cyclase activity in lysates from lymphocytes exposed to the invasive enzyme is insensitive to N-ethylmaleimide, readily inactivated by acetic anhydride and relatively stable to SDS. Similar properties are exhibited by the bacterial enzyme itself. By contrast, the intrinsic membrane-bound enzyme activated by forskolin and guanosine 5'-gamma-thiotriphosphate is sensitive to N-ethylmaleimide and SDS and relatively stable to acetic anhydride. This strongly supports the notion that B. pertussis adenylate cyclase penetrates cells. Using the partially purified preparation of the invasive enzyme, we have studied the kinetics of its penetration. The intracellular catalytic activity reaches a steady state within 20 min, irrespective of enzyme or cell concentration. Steady-state levels are maintained for at least 2 h provided that the invasive enzyme is present in the incubation medium. Upon its removal, a rapid decrease (t1/2 approximately equal to 15 min) in the intracellular cyclase level is observed. This decrease reflects intracellular inactivation of the bacterial enzyme and is not caused by the release of the enzyme to the cell medium.
百日咳博德特氏菌是百日咳的病原体,可产生一种钙调蛋白敏感的腺苷酸环化酶。康弗尔和伊顿[(1982年)《科学》217卷,948 - 950页]已经表明,百日咳博德特氏菌的提取物会增加中性粒细胞内的环磷酸腺苷(cAMP)水平,并提出这种增加是由穿透这些细胞的细菌腺苷酸环化酶引起的。我们在本研究中证明,暴露于该细菌酶部分纯化制剂的淋巴细胞裂解物中的腺苷酸环化酶活性,其性质与内在膜结合酶的性质完全不同。暴露于侵袭性酶的淋巴细胞裂解物中的腺苷酸环化酶活性对N - 乙基马来酰亚胺不敏感,易被乙酸酐灭活,且对十二烷基硫酸钠(SDS)相对稳定。细菌酶本身也表现出类似的性质。相比之下,由福司可林和鸟苷5'-γ-硫代三磷酸激活的内在膜结合酶对N - 乙基马来酰亚胺和SDS敏感,对乙酸酐相对稳定。这有力地支持了百日咳博德特氏菌腺苷酸环化酶穿透细胞的观点。使用侵袭性酶的部分纯化制剂,我们研究了其穿透动力学。无论酶或细胞浓度如何,细胞内催化活性在20分钟内达到稳态。只要孵育培养基中存在侵袭性酶,稳态水平就能维持至少2小时。去除该酶后,观察到细胞内环化酶水平迅速下降(半衰期约为15分钟)。这种下降反映了细菌酶在细胞内的失活,而不是由于酶释放到细胞培养基中所致。