Soong M M, Iijima S, Wang L H
J Virol. 1986 Sep;59(3):556-63. doi: 10.1128/JVI.59.3.556-563.1986.
The mechanism of cellular src (c-src) transduction by a transformation-defective deletion mutant, td109, of Rous sarcoma virus was studied by sequence analysis of the recombinational junctions in three td109-derived recovered sarcoma viruses (rASVs). Our results show that two rASVs have been generated by recombination between td109 and c-src at the region between exons 1 and 2 defined previously. Significant homology between td109 and c-src sequences was present at the sites of recombination. The viral and c-src sequence junction of the third rASV was formed by splicing a cryptic donor site at the 5' region of env of td109 to exon 1 of c-src. Various lengths of c-src internal intron 1 sequences were incorporated into all three rASV genomes, which resulted from activation of potential splice donor and acceptor sites. The incorporated intron 1 sequences were absent in the c-src mRNA, excluding its being the precursor for recombination with td109 and implying that initial recombinations most likely took place at the DNA level. A potential splice acceptor site within the incorporated intron 1 sequences in two rASVs was activated and was used for the src mRNA synthesis in infected cells. The normal env mRNA splice acceptor site was used for src mRNA synthesis for the third rASV.
通过对三种源自td109的恢复性肉瘤病毒（rASV）中重组连接点的序列分析，研究了劳斯肉瘤病毒的转化缺陷型缺失突变体td109介导的细胞src（c-src）转导机制。我们的结果表明，两种rASV是由td109和c-src在先前定义的外显子1和2之间的区域发生重组产生的。在重组位点存在td109和c-src序列之间的显著同源性。第三种rASV的病毒和c-src序列连接是通过将td109 env 5'区域的一个隐蔽供体位点剪接到c-src的外显子1上形成的。各种长度的c-src内部内含子1序列被整合到所有三种rASV基因组中，这是由潜在的剪接供体和受体位点的激活导致的。c-src mRNA中不存在整合的内含子1序列，这排除了其作为与td109重组的前体的可能性，并暗示最初的重组很可能发生在DNA水平。两种rASV中整合的内含子1序列内的一个潜在剪接受体位点被激活，并用于感染细胞中src mRNA的合成。第三种rASV的src mRNA合成使用正常的env mRNA剪接受体位点。
