Cremisi C, Babinet C
J Virol. 1986 Sep;59(3):761-3. doi: 10.1128/JVI.59.3.761-763.1986.
Embryonal carcinoma cells are resistant to infection by polyomavirus (Py). We showed that this block was partially removed by inhibiting protein synthesis temporarily. The block was also partially removed when Py was coinfected with simian virus 40. Cycloheximide treatment of cells infected with Py mutants able to grow on PCC4 embryonal carcinoma cells led to 3- to 10-fold increases in the production of T-antigen-positive cells. At 31 degrees C, Py T-antigen expression was enhanced when the cells were treated with cycloheximide. We suggest that a negative labile regulatory protein(s) is synthesized in PCC4 cells, preventing the initiation of early Py transcription by binding to the noncoding sequence, especially the enhancer element B and perhaps also element A, and that the Py mutants retained a binding site(s).
胚胎癌细胞对多瘤病毒(Py)感染具有抗性。我们发现,通过暂时抑制蛋白质合成可部分消除这种阻断作用。当Py与猿猴病毒40共同感染时,这种阻断也会部分消除。用环己酰亚胺处理感染了能在PCC4胚胎癌细胞上生长的Py突变体的细胞,会使T抗原阳性细胞的产生增加3至10倍。在31摄氏度时,用环己酰亚胺处理细胞会增强Py T抗原的表达。我们认为,PCC4细胞中合成了一种不稳定的负调控蛋白,它通过与非编码序列(尤其是增强子元件B,可能还有元件A)结合来阻止Py早期转录的起始,并且Py突变体保留了一个结合位点。