首页> 美国卫生研究院文献>Journal of Virology >Genome structure of mink cell focus-forming murine leukemia virus in epithelial mink lung cells transformed vitro by iododeoxyuridine-induced C3H/MuLV cells.
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Genome structure of mink cell focus-forming murine leukemia virus in epithelial mink lung cells transformed vitro by iododeoxyuridine-induced C3H/MuLV cells.

机译:由碘脱氧尿苷诱导的C3H / MuLV细胞体外转化的上皮水貂肺细胞中水貂细胞聚焦形成鼠白血病病毒的基因组结构。

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摘要

We characterized mink cell focus-forming murine leukemia viruses that were isolated from C3H/MCA-5 cells after induction with 5-iododeoxyuridine in culture. Mink lung epithelial cells malignantly transformed in vitro by induced virus were the source of four molecular clones of mink cell focus-forming virus. CI-1, CI-2, CI-3, and CI-4. Three clones, CI-1, CI-2, and CI-3, had full-length mink cell focus-forming viral genomes, one of which (CI-3) was infectious. In addition, we obtained a defective viral genome (CI-4) which had a deletion in the envelope gene. A comparison between the envelope genes of CI-4 and those of spleen focus-forming virus by heteroduplex mapping showed close homology in the substitution region and defined the deletion as being identical to the p15E deletion of spleen focus-forming virus. The recombinant mink cell focus-forming genomes are not endogenous in C3H/MCA-5 cells and therefore must have been formed in culture after induction by 5-iododeoxyuridine. CI-3, the infectious clone of mink cell focus-forming murine leukemia virus, was dualtropic, and mink cells infected with CI-3 were altered in their response to epidermal growth factor. In the presence of epidermal growth factor at 10 ng/ml, uninfected mink cells retained their epithelial morphology in monolayer culture and did not form colonies in soft agar. In contrast, CI-3 virus-infected mink cells grew with fibroblastic morphology in monolayer culture and showed an increased growth rate in soft agar in the presence of epidermal growth factor.
机译:我们表征了形成水貂细胞焦点的鼠类白血病病毒,该病毒是在培养物中用5-碘脱氧尿苷诱导后从C3H / MCA-5细胞中分离出来的。水貂肺上皮细胞在体外被诱导的病毒恶性转化,是水貂细胞聚焦形成病毒四个分子克隆的来源。 CI-1,CI-2,CI-3和CI-4。三个克隆CI-1,CI-2和CI-3具有全长形成貂细胞焦点的病毒基因组,其中一个(CI-3)具有传染性。此外,我们获得了有缺陷的病毒基因组(CI-4),其包膜基因有缺失。通过异源双链作图对CI-4的包膜基因和脾脏形成灶病毒的包膜基因进行比较,显示在置换区域具有紧密的同源性,并且将该缺失定义为与脾脏形成灶病毒的p15E缺失相同。重组貂细胞焦点形成基因组在C3H / MCA-5细胞中不是内源的,因此必须在5-碘脱氧尿苷诱导后在培养中形成。 CI-3是形成貂细胞病灶的鼠白血病病毒的传染性克隆,是双向性的,感染了CI-3的貂细胞对表皮生长因子的反应发生了改变。在表皮生长因子为10 ng / ml的情况下,未感染的貂细胞在单层培养中保持其上皮形态,在软琼脂中不形成菌落。相反,CI-3病毒感染的貂细胞在单层培养中以成纤维细胞形态生长,并且在存在表皮生长因子的情况下在软琼脂中显示出增加的生长速率。

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