Yang F, Lazzarini R A
J Virol. 1983 Feb;45(2):766-72. doi: 10.1128/JVI.45.2.766-772.1983.
cDNA clones of different portions of the L cistron and 5'-terminal region of the vesicular stomatitis virus genome have been prepared and used to identify the exact site of the deletion in the defective interfering particle, DI-LT. The deletion extends from nucleotide 251 from the beginning of the L gene to a position 342 nucleotides from the end of the genome. The nucleotide sequences flanking the deletion site, as well as those at the ends of the deleted segment, did not contain any obvious vesicular stomatitis virus initiation or termination signals as had been found near the recombination sites in other defective interfering particle RNAs. The results best fit a model for the origin of this type of defective interfering particle in which the polymerase interrupts its synthesis and moves with its nascent daughter strand to a new position on the template and resumes synthesis there, further extending the nascent strand. Neither the interruption nor the resumption of synthesis appears to be in response to the template nucleotide sequence. The sequences of two partial L cistron clones also reveal open reading frames that code for amino acid sequences likely to be the amino and carboxy termini of the L protein.
水泡性口炎病毒基因组L顺反子不同部分和5'末端区域的cDNA克隆已制备完成,并用于确定缺陷干扰颗粒DI-LT中缺失的确切位点。该缺失从L基因起始处的第251个核苷酸延伸至基因组末端342个核苷酸处。缺失位点两侧的核苷酸序列,以及缺失片段末端的序列,均未包含任何明显的水泡性口炎病毒起始或终止信号,而在其他缺陷干扰颗粒RNA的重组位点附近曾发现过此类信号。这些结果最符合这种类型的缺陷干扰颗粒的起源模型,即聚合酶中断其合成,并与其新生子链一起移动到模板上的新位置,然后在那里恢复合成,进一步延伸新生链。合成的中断和恢复似乎都不响应模板核苷酸序列。两个部分L顺反子克隆的序列还揭示了开放阅读框,其编码的氨基酸序列可能是L蛋白的氨基末端和羧基末端。