Feunteun J, Kress M, Gardes M, Monier R
Proc Natl Acad Sci U S A. 1978 Sep;75(9):4455-9. doi: 10.1073/pnas.75.9.4455.
For the purpose of isolating hr-t-like mutants of simian virus 40, we have constructed variants that have lost the unique site for the restriction enzyme Taq I at 0.565. Five mutants have been isolated and characterized by restriction enzyme analysis. All of them produce a normal size T antigen. Four produce a t antigen reduced in size as well as in amount; the fifth one does not seem to make any t antigen at all. The ability of these mutants to transform mouse cells in vitro, as tested by anchorage dependence, is clearly altered; however, the defect is only partial. In the same test, the mutants can complement a tsA mutant for transformation and therefore define a second complementation group in the simian virus 40 early region.
为了分离猿猴病毒40(SV40)的hr-t样突变体,我们构建了在0.565处失去限制性内切酶Taq I独特位点的变体。已分离出五个突变体,并通过限制性内切酶分析进行了表征。它们都产生正常大小的T抗原。四个突变体产生大小和数量都减少的t抗原;第五个突变体似乎根本不产生任何t抗原。通过锚定依赖性测试,这些突变体在体外转化小鼠细胞的能力明显改变;然而,缺陷只是部分的。在同一测试中,这些突变体可以互补tsA突变体进行转化,因此在猿猴病毒40早期区域定义了第二个互补组。