Nunn M F, Hunter T
Molecular Biology and Virology Laboratory, Salk Institute, San Diego, California 92138-9216.
J Virol. 1989 Jan;63(1):398-402. doi: 10.1128/JVI.63.1.398-402.1989.
E26 is a replication-defective avian retrovirus that causes an erythroblastic leukemia in vivo and transforms hematopoietic precursor cells of both the erythroid and the myeloid lineages in vitro. The E26 genome contains two sets of cell-derived sequences, ets and myb. myb sequences are also present in avian myeloblastosis virus, which transforms myeloblasts exclusively. To determine whether the ets sequence is responsible for the erythroid specificity of E26, we analyzed the transforming activities of several viruses carrying mutations in the ets sequence constructed in vitro. The mutant viruses retained the ability to transform myeloid cells in vitro, indicating that the myb oncogene is sufficient for this viral function. However, the ets-deficient viruses did not cause an overt leukemia in chickens. The results indicate that the ets sequence is required for the induction of erythroblastosis by E26.
E26是一种复制缺陷型禽逆转录病毒,它在体内可引发成红细胞性白血病,在体外可转化红系和髓系造血前体细胞。E26基因组包含两组细胞来源的序列,即ets和myb。myb序列也存在于禽成髓细胞瘤病毒中,该病毒仅转化成髓细胞。为了确定ets序列是否对E26的红系特异性负责,我们分析了几种在体外构建的携带ets序列突变的病毒的转化活性。突变病毒在体外保留了转化髓细胞的能力,这表明myb癌基因足以实现这种病毒功能。然而,缺乏ets的病毒在鸡中并未引发明显的白血病。结果表明,E26诱导成红细胞增多症需要ets序列。