STUDIES OF E26 AVIAN V-ETS AND ITS CELLULAR HOMOLOGUE IN MOUSE CELLS

禽急性白血病病毒E26表达致癌融合蛋白 含有来自禽类的myb和ets-1基因的部分 基因组 为了研究正常和致癌功能， 这些基因，特别是ets，我们已经开发了一种小鼠模型， 通过引入gag-myb-ets编码序列从 E26转化到鼠逆转录病毒载体中。 这种缺陷鼠病毒 构建体（ME 26）在新生小鼠中诱导白血病并消除血清 NIH 3 T3鼠成纤维细胞生长的依赖性。 我们现在已经分析了NIH 3 T3细胞中血清应答基因的表达， 已经失去对血清生长依赖性的成纤维细胞 感染ME 26后。 fos，jun或myc表达无增加 与未感染的3 T3细胞相比，在ME 26感染的细胞中观察到， 并且在ME 26感染的造血细胞中的表达也没有改变。 同样，c-ets-I和c-ets-2的内源性表达也没有增加。 这些细胞。 这些结果表明，ME 26可能诱导 成纤维细胞中的血清非依赖性生长的机制， 涉及血清反应途径。 我们还发现了一个新的3.7 kb的亚基因组ME 26信息， 感染的成纤维细胞和造血细胞。 亚基因组 消息包含myb和v-ets特定的序列， 被整合到病毒颗粒中。 这个的编码潜力 亚基因组信息仍有待确定。

The avian acute leukemia virus, E26, expresses oncogenic fusion proteins containing portions of the myb and ets-1 genes derived from the avian genome. In order to study both the normal and oncogenic functions of these genes, particularly ets, we have developed a murine model for myb-ets oncogenesis by introducing the gag-myb-ets coding sequences from E26 into a murine retroviral vector. This defective murine viral construct (ME26) induces leukemia in newborn mice and abrogates the serum dependence for growth of NIH3T3 murine fibroblasts. We have now analyzed the expression of serum-response genes in NIH3T3 fibroblasts which have lost their dependence on serum for growth following infection of ME26. No increase in fos, jun or myc expression was seen in ME26-infected cells in comparison to uninfected 3T3 cells, and expression in ME26-infected hematopoietic cells was also not altered. Likewise, c-ets-I and c-ets-2 endogenous expression was not increased in these cells. These results suggest that ME26 may induce serum-independent growth in fibroblasts by a mechanism that does not involve the serum-response pathway. We have also detected a novel 3.7 kb subgenomic ME26 message in both infected fibroblasts and hematopoietic cells in culture. The subgenomic message contains both myb and v-ets specific sequences and is not incorporated into viral particles. The coding potential of this subgenomic message remains to be determined.