GENETIC ASPECTS OF VIRAL ONCOGENESIS IN WILD MOUSE SPECIES AND LABORATORY MICE

许多与病毒诱导的肿瘤性疾病有关的小鼠基因， 在遗传学研究中被发现。 这些基因包括内源性 逆转录病毒序列以及促进或 抑制病毒复制。 我们把人类基因用在了巨猿身上 白血病病毒（GALV）受体，以确定同源序列中的 小鼠，我们还确定了多个拷贝的GALV相关序列 在小鼠的基因组中，这表明该基因可能起着 我们对这一序列的基因图谱 也表明可能与Rec-2相同， 野生小鼠逆转录病毒的研究 在其他实验中， 三个与肿瘤诱导相关的常见病毒整合区， 证明一个代表一个新的基因，一个代表一个新的基因。 先前显示的位点在整合后被重排， 不同的病毒，导致不同的疾病类型。 我们也 表明Fv-2抗性基因座不编码 红细胞生成素受体，但确定了一个基因组序列， 或者在这个抗性基因附近 最后，我们使用了特定于站点的 突变以改变AKV MuLV的p30 gag区中的位点 它被认为与Fv-1的基因产物相互作用， 抗性基因

Numerous mouse genes involved in virus-induced neoplastic disease have been identified in genetic studies. These genes include endogenous retroviral sequences as well as mouse cellular genes which facilitate or inhibit virus replication. We used the human gene for the gibbon ape leukemia virus (GALV) receptor to identify homologous sequences in the mouse, and we also identified multiple copies of GALV-related sequences in the mouse genome suggesting that this gene may have functioned as a receptor in the evolution of Mus. Our genetic mapping of this sequence also suggested possible identity with Rec-2, the Chr 2 encoded receptor for a wild mouse retrovirus. In other experiments we characterized three common viral integration regions associated with tumor induction, demonstrating that one represents a novel gene, and one represents a site previously shown to be rearranged following integration by a different virus and resulting in a different disease type. We also demonstrated that the Fv-2 resistance locus does not encode the erythropoietin receptor, but identified a genomic sequence which maps at or near this resistance gene. Finally, we have used site specific mutagenesis to alter the site in the p30 gag region of the AKV MuLV which is thought to interact with the gene product of the Fv-1 resistance gene.