Defective interfering influenza RNAs of polymerase 3 gene contain single as well as multiple internal deletions.

Defective interfering influenza RNAs of polymerase 3 gene contain single as well as multiple internal deletions.
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聚合酶 3 基因有缺陷的干扰性流感 RNA 含有单个和多个内部缺失。

DOI:
10.1016/0042-6822(83)90340-9
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发表时间:
1983
期刊:
影响因子:
3.7
通讯作者:
Nayak,DP
Nayak,DP
中科院分区:
医学3区
文献类型:
--
作者:
Sivasubramanian,N;Nayak,DP

文献摘要

被引文献

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流感病毒的缺陷性干扰(DI)RNA通过内部缺失由聚合酶基因产生。利用重组DNA克隆和测序技术,我们确定了A/WSN/33的L克隆的两个DI RNA(L2 a-7和L2 a-17)的核苷酸序列,这两个DI RNA是聚合酶3来源的。L2 a-7 DI RNA长659个核苷酸,含有P3基因的1682个核苷酸(核苷酸位置273至1954)的单个内部缺失。而L2 a-17 DI RNA(611个核苷酸长)含有两个内部缺失:一个在与L2 a-7相同的1682个核苷酸的位置处,另一个在P3基因的核苷酸位置2032至2079处的48个核苷酸。除少数碱基错配外,DI RNA的序列与P3基因的相应部分(包括5′和3′末端)相同。由于这两个DI RNA含有一个相同的缺失,但在另一个缺失以及碱基错配方面不同,因此这两个DI RNA似乎起源于祖先DI RNA,而不是独立于祖先P3基因。缺失点周围的序列不反映这些缺失起源的共有序列,并表明多种机制在流感DI RNA的产生和进化中的作用。
Defective interfering (DI) RNAs of influenza virus arise from polymerase genes by internal deletions. Utilizing the recombinant DNA cloning and sequencing techniques we have determined the nucleotide sequence of two DI RNAs of L clone of A/WSN/33 (L2a-7 and L2a-17) which are of polymerase 3 origin. L2a-7 DI RNA is 659 nucleotides long and contains a single internal deletion of 1682 nucleotides (nucleotide position 273 to 1954) of P3 gene. L2a-17 DI RNA (611 nucleotides long), on the other hand, contains two internal deletions: one of 1682 nucleotides at the identical position as that in L2a-7, the other 48 nucleotides at the nucleotide position 2032 to 2079 of P3 gene. Except for a few base mismatches the sequence of DI RNAs are identical to the corresponding portion of the P3 gene including the 5′ and the 3′ termini. Since these two DI RNAs contain one identical deletion but differ in the other deletion as well as in base mismatches, these two DI RNAs appear to originate from a progenitor DI RNA rather than independently from the progenitor P3 gene. The sequences around the deletion point do not reflect a consensus sequence for the origin of these deletions and suggest the role of multiple mechanisms in the generation and evolution of influenza DI RNAs.