Nayak D P, Sivasubramanian N, Davis A R, Cortini R, Sung J
Proc Natl Acad Sci U S A. 1982 Apr;79(7):2216-20. doi: 10.1073/pnas.79.7.2216.
Defective interfering (DI) influenza viral RNAs arise by internal deletion of progenitor RNAs. By using recombinant DNA cloning and DNA sequence analysis techniques, we have deduced the complete sequence of two such RNAs (L2b and L3), both arising from the same polymerase (P1) gene of WSN influenza virus. We have also partially determined the sequence of the P1 polymerase gene, including the sequence at the point of deletion and the flanking regions. Our sequence study shows the following. (i) Both L2b and L3 arise by a simple deletion in the P1 gene. (ii) L2b and L3 are 683 and 441 nucleotides long, respectively. (iii) The first 413 and 244 nucleotides of the 5' ends of L2b and L3, respectively, are identical to those of the 5' end of the P1 gene. (iv) The last 270 nucleotides of L2b and 197 nucleotides of L3 are the same as those of the 3' end of the P1 gene. (v) The entire sequence of L3 is present in the sequence of L2b. (vi) Both the 5' and the 3' termini, including the transcription stop and poly(A) addition signals of the progenitor P1 gene, are present in both L2b and L3. (vii) The sequences at the deletion point and the flanking region of the P1 gene do not resemble the consensus splicing sequence of spliced mRNA suggesting that a replicational event rather than splicing is involved in the formation of influenza defective interfering RNAs.
缺陷干扰（DI）流感病毒RNA是由祖代RNA的内部缺失产生的。通过使用重组DNA克隆和DNA序列分析技术，我们已经推导了两种这样的RNA（L2b和L3）的完整序列，它们均来自WSN流感病毒的同一聚合酶（P1）基因。我们还部分确定了P1聚合酶基因的序列，包括缺失点及其侧翼区域的序列。我们的序列研究表明如下几点。（i）L2b和L3均由P1基因中的简单缺失产生。（ii）L2b和L3分别长683和441个核苷酸。（iii）L2b和L3 5'端的前413和244个核苷酸分别与P1基因5'端的核苷酸相同。（iv）L2b的最后270个核苷酸和L3的197个核苷酸与P1基因3'端的核苷酸相同。（v）L3的整个序列存在于L2b的序列中。（vi）L2b和L3中均存在5'和3'末端，包括祖代P1基因的转录终止和聚腺苷酸化信号。（vii）P1基因缺失点及其侧翼区域的序列与剪接mRNA的共有剪接序列不同，这表明流感缺陷干扰RNA的形成涉及复制事件而非剪接。
