首页> 美国卫生研究院文献>Proceedings of the National Academy of Sciences of the United States of America >Complete sequence analyses show that two defective interfering influenza viral RNAs contain a single internal deletion of a polymerase gene.
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Complete sequence analyses show that two defective interfering influenza viral RNAs contain a single internal deletion of a polymerase gene.

机译:完整的序列分析表明两个有缺陷的干扰流感病毒RNA包含一个聚合酶基因的单个内部缺失。

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摘要

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.
机译:缺陷干扰(DI)流感病毒RNA由祖RNA的内部缺失引起。通过使用重组DNA克隆和DNA序列分析技术,我们推导出了两个此类RNA的完整序列(L2b和L3),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,包括缺失点和侧翼区域的序列。我们的序列研究显示以下内容。 (i)L2b和L3都通过P1基因的简单缺失而产生。 (ii)L2b和L3分别长683和441个核苷酸。 (iii)L2b和L3的5'端的前413和244个核苷酸分别与P1基因的5'端相同。 (iv)L2b的最后270个核苷酸和L3的197个核苷酸与P1基因的3'末端的相同。 (v)L3的整个序列存在于L2b的序列中。 (vi)L2b和L3均存在5'和3'末端,包括祖先P1基因的转录终止和poly(A)添加信号。 (vii)在P1基因的缺失点和侧翼区域的序列与剪接的mRNA的共有剪接序列不同,这表明复制事件而不是剪接参与流感缺陷型干扰RNA的形成。

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