Azarnia R, Loewenstein W R
J Membr Biol. 1984;82(3):213-20. doi: 10.1007/BF01871631.
We studied the action of temperature-sensitive mutant simian virus 40--a transformation-inducing DNA virus--on the junctional permeability to mono-, di- and triglutamate in rat embryo-, pancreas islet (epithelial)-, and 10T1/2 cell cultures. Junctional permeability was reduced (reversibly) in the transformed state. To dissect the genetics of this alteration, we used two kinds of mutant virus DNA. One kind had a temperature-sensitive mutation on the A gene, rendering the large T antigen (the gene product) thermolabile (T+ in equilibrium T-). The other had a deletion on the F gene, in addition, abolishing (permanently) the expression of the little t addition (t-). The junctional alteration occurred in the condition T+ t+, but not in the conditions T- t+, T+ t- or T- t-. Both antigens, thus, are necessary for this junctional alteration--a genetic requirement identical to that for decontrol of growth (but distinct from that of the cytoskeletal alteration).
我们研究了温度敏感突变型猿猴病毒40(一种诱导转化的DNA病毒)对大鼠胚胎、胰岛(上皮)和10T1/2细胞培养物中连接对单谷氨酸、二谷氨酸和三谷氨酸通透性的影响。在转化状态下,连接通透性降低(可逆)。为了剖析这种改变的遗传学机制,我们使用了两种突变病毒DNA。一种在A基因上有温度敏感突变,使大T抗原(基因产物)热不稳定(T+处于平衡的T-状态)。另一种在F基因上有缺失,此外,消除(永久)了小t抗原的表达(t-)。连接改变发生在T+ t+条件下,而在T- t+、T+ t-或T- t-条件下未发生。因此,两种抗原对于这种连接改变都是必需的——这一遗传学要求与生长失控的要求相同(但与细胞骨架改变的要求不同)。