首页> 美国卫生研究院文献>Journal of Virology >Characterization of a Rous sarcoma virus mutant defective in packaging its own genomic RNA: biological properties of mutant TK15 and mutant-induced transformants.
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Characterization of a Rous sarcoma virus mutant defective in packaging its own genomic RNA: biological properties of mutant TK15 and mutant-induced transformants.

机译:Rous肉瘤病毒突变体的特征在于包装其自身的基因组RNA缺陷:突变体TK15和突变体诱导的转化子的生物学特性。

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摘要

A mutant derived from a temperature-sensitive mutant of Rous sarcoma virus ( tsNY68 ) which showed extremely low infectivity was characterized. Infection of chicken embryo fibroblast cells with the mutant, TK15 , induced two types of transformants, mutant-producing 15c (+) and nonvirus -producing 15c (-) transformants. 15c (+) cells expressed all four viral genes normally and produced a normal level of virus particles. No complementation was observed between the mutant and avian leukosis viruses. However, when 15c (+) cells were cocultured with nonvirus -producing cells transformed by Y73, a replication-defective avian sarcoma virus, a high titer of Y73 virus was recovered. From its biological properties, the mutant seemed to have a defect(s) outside the viral genes. Biochemical analysis of the TK15 mutant (T. Koyama , F. Harada, and S. Kawai , J. Virol. 51:154-162, 1984) revealed that it had a defect in packaging its own genomic RNA. During replication of TK15 virus, the TK15 mutant appeared to segregate at high frequency more defective variants that induced 15c (-) transformants, in most of which only the src gene was expressed. The mechanism for the segregation of 15c (-) transformants is discussed with respect to the defect of the mutant.
机译:表征了衍生自劳斯肉瘤病毒(tsNY68)的温度敏感性突变体的突变体,该突变体显示出极低的感染性。用突变体TK15感染鸡胚成纤维细胞会诱导两种类型的转化子,即产生突变体的15c(+)和不产生病毒的15c(-)转化子。 15c(+)细胞正常表达所有四个病毒基因,并产生正常水平的病毒颗粒。在突变型和禽白血病病毒之间未观察到互补。但是,当将15c(+)细胞与由复制缺陷型禽肉瘤病毒Y73转化的非病毒产生细胞共培养时,可以回收到高滴度的Y73病毒。从其生物学特性来看,该突变体似乎在病毒基因之外具有缺陷。对TK15突变体(T.Koyama,F.Harada,和S.Kawai,J.Virol.51:154-162,1984)的生化分析表明,它在包装自己的基因组RNA方面有缺陷。在TK15病毒复制过程中,TK15突变体似乎在高频下分离出更多有缺陷的变异体,这些变异体诱导15c(-)转化子,其中大多数仅表达src基因。关于突变体的缺陷,讨论了分离15c(-)转化子的机制。

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