PESTICINS .3. EXPRESSION OF COAGULASE AND MECHANISM OF FIBRINOLYSIS
PESTICINS .3. EXPRESSION OF COAGULASE AND MECHANISM OF FIBRINOLYSIS
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DOI：
10.1128/jb.94.1.19-26.1967
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发表时间：
1967-01-01
影响因子：
3.2
通讯作者：
SURGALLA, MJ
中科院分区：
文献类型：
--
作者：
BEESLEY, ED;BRUBAKER, RR;SURGALLA, MJ
已知鼠疫杆菌产生的一种类似细菌素的物质--pesticin-I的突变丢失会导致凝固酶和纤溶因子的伴随丢失。未发现鼠疫菌致病性与其他与毒力相关或鼠疫菌特有的测试特性之间的关系。基于解剖学分布、凝胶过滤过程中的行为和对热的敏感性，将Pesticin-I与凝固酶和纤溶活性区分开。这些标准不能区分凝血酶和纤溶因子。未检测到自发的抑制突变引起pesticinestrin逆转，也没有这样的突变体通过紫外线或2-氨基嘌呤治疗获得。试图证明一个共同的激活剂pesticin-I，凝固酶，或纤维蛋白溶解因子的pesticinogenic细胞提取物没有成功。这些结果与以下假设雅阁：至少有两个与这三种活性相关的结构基因位于与染色体本身不同的复制子上。纤溶活性显着降低，在0。003 M ε-氨基己酸，并不存在于通过加热处理从内源性纤溶酶原释放的纤维蛋白膜上。加热膜上的纤溶活性可以通过添加六种哺乳动物的血浆或血清来恢复。因此，鼠疫纤溶因子，如葡激酶或尿激酶，促进纤溶酶原转化为纤溶酶。
Mutational loss of pesticin-I, a bacteriocin-like substance produced by Pasteurella pestis, is known to result in concomitant loss of a coagulase and fibrinolytic factor. No relationship was detected between pestici-nogeny and other tested properties either associated with virulence or peculiar to P. pestis. Pesticin-I was distinguished from the coagulase and fibrinolytic activities on the basis of anatomical distribution, behavior during gel filtration, and sensitivity to heat. Coagulase and fibrinolytic factor were not differentiated by these criteria. Spontaneous suppressor mutations causing reversion to pesticinogeny were not detected, nor were such mutants obtained by treatment with ultraviolet light or 2-aminopurine. Attempts to demonstrate a common activator of pesticin-I, coagulase, or the fibrinolytic factor in extracts of pesticinogenic cells were not successful. These results are in accord with the hypothesis that at least two structural genes for the three activities reside on a replicon distinct from the chromosome proper. Fibrinolytic activity was significantly reduced in the presence of 0. 003 M epsilon-aminocaproic acid and was nonexistent on fibrin films freed from endogenous plasminogen by treatment with heat. Fibrinolytic activity on heated films could be restored by addition of plasma or serum from six mammalian species. Accordingly, the plague fibrinolytic factor, like staphylokinase or urokinase, promotes the conversion of plasminogen to plasmin.