Tosu M, Tanooka H
Radiobiology Division, National Cancer Center Research Institute, Tokyo, Japan.
Mol Cell Biol. 1990 Oct;10(10):5359-64. doi: 10.1128/mcb.10.10.5359-5364.1990.
The enterobacterial plasmid misrepair gene mucAB, ligated to the metal-inducible mammalian MT-1 promoter, was introduced into the genome of mouse BALB 3T3 cells. In the presence of zinc ions, MucA but not MucB protein was produced, and the whole-cell population of each mucAB+ clone started to show the transformation phenotype in a few days. Foci appeared in the transformed cell population after 4 weeks, and cells from the foci produced tumors in nude mice, indicating malignant transformation by the mucA product. Growth of mucAB+ cells was stimulated by zinc-induced expression of mucA. The transformation phenotype was reversed by removing zinc ions from the culture, indicating that the transformation was due not to MucA-mediated mutation in the mouse genome but to the direct transforming activity of MucA protein.
将连接到金属诱导型哺乳动物MT-1启动子上的肠杆菌质粒错配修复基因mucAB导入小鼠BALB 3T3细胞基因组。在锌离子存在的情况下,产生了MucA蛋白而非MucB蛋白,每个mucAB +克隆的全细胞群体在几天内开始表现出转化表型。4周后在转化细胞群体中出现病灶,病灶中的细胞在裸鼠中产生肿瘤,表明mucA产物导致了恶性转化。锌诱导的mucA表达刺激了mucAB +细胞的生长。从培养物中去除锌离子可逆转转化表型,这表明转化不是由于小鼠基因组中MucA介导的突变,而是由于MucA蛋白的直接转化活性。