Ramsay G M, Hayman M J
J Virol. 1982 Mar;41(3):745-53. doi: 10.1128/JVI.41.3.745-753.1982.
Recently, we isolated three mutants of MC29 virus which, although able to transform fibroblasts with the same efficiency as wild-type MC29, were 100-fold less efficient at transforming macrophages. In this study we found that MC29-transformed quail producer cell line Q10 was able to generate these partially transformation defective mutants at a high frequency. Using tryptic peptide mapping, we determined that the smaller gag-myc polyproteins encoded by the transformation-defective viruses had lost myc-specific tryptic peptides. This suggested that the mutations which resulted in the transformation-defective viruses being inefficient at transforming macrophages were located in the v-myc sequence and thus directly implicated v-myc and the gag-myc polyprotein in transformation by MC29.
最近，我们分离出了三种MC29病毒突变体，它们虽然能够以与野生型MC29相同的效率转化成纤维细胞，但在转化巨噬细胞方面的效率却低100倍。在本研究中，我们发现MC29转化的鹌鹑生产细胞系Q10能够高频产生这些部分转化缺陷型突变体。通过胰蛋白酶肽图谱分析，我们确定转化缺陷型病毒编码的较小的gag-myc多聚蛋白失去了myc特异性胰蛋白酶肽段。这表明导致转化缺陷型病毒在转化巨噬细胞方面效率低下的突变位于v-myc序列中，因此直接表明v-myc和gag-myc多聚蛋白参与了MC29的转化过程。
