Enrietto P J, Hayman M J
Proc R Soc Lond B Biol Sci. 1985 Oct 22;226(1242):83-92. doi: 10.1098/rspb.1985.0082.
We describe the generation and characterization of a series of deletion mutants of the avian acute leukaemia virus MC29 which allow the study of the function of the myc in transformation of quail embryo fibroblasts in vitro and tumour induction in vivo. These mutants, which are deleted in the 3' portion of the myc gene, fail to transform macrophages in vitro or induce tumours in vivo but are still able to transform morphologically fibroblasts. From one of these mutants a 'recovered' MC29 virus was generated which, like wild type MC29, transformed fibroblasts and macrophages in vitro. When tested in vivo this virus induced lymphomas of T and B cells rather that the endotheliomas induced by wild type MC29. This system allows us to investigate another question which is the mechanism by which the virus (or oncogene it contains) preferentially transforms one cell type.
我们描述了一系列禽急性白血病病毒MC29缺失突变体的产生和特性，这些突变体有助于研究myc在体外转化鹌鹑胚胎成纤维细胞以及体内诱导肿瘤过程中的功能。这些突变体在myc基因的3'部分缺失，无法在体外转化巨噬细胞或在体内诱导肿瘤，但仍能够在形态上转化成纤维细胞。从其中一个突变体产生了一种“恢复型”MC29病毒，它与野生型MC29一样，能在体外转化成纤维细胞和巨噬细胞。在体内测试时，这种病毒诱导T细胞和B细胞淋巴瘤，而不是野生型MC29诱导的内皮瘤。这个系统使我们能够研究另一个问题，即病毒（或其所含的癌基因）优先转化一种细胞类型的机制。
