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在缺陷病毒和猿猴肉瘤病毒中发现了猿猴肉瘤相关病毒基因组特定区域的缺失。

Deletions of specific regions of the simian sarcoma-associated virus genome are found in defective viruses and in the simian sarcoma virus.

作者信息

Gelmann E P, Petri E, Cetta A, Wong-Staal F

出版信息

J Virol. 1982 Feb;41(2):593-604. doi: 10.1128/JVI.41.2.593-604.1982.

Abstract

Extrachromosomal DNA was isolated from tissue culture cells that were acutely infected with simian sarcoma virus (SSV) and its associated helper (simian sarcoma-associated virus [SSAV]). Two sizes of closed circular viral genomic DNA intermediates were isolated, cleaved at the single EcoRI site, and ligated to the Charon 21A phage lambda vector. Cloned molecules of the larger size all represented the full-length (9.0-kilobase [kb]) SSAV molecule. A heterogeneous group of clones was derived from the smaller DNA circles. These included the SSV genome and SSAV deletion mutants. When two SSV clones were compared with the helper, they contained the following three characteristic deletions: (i) a 250-base pair deletion in the gag gene about 1.0 kb from the 5' end of the genome; (ii) a 1.85-kb deletion in the pol gene; and (iii) a 1.9-kb deletion at the 3' end, which included part of the env gene. This latter deletion was the site of the onc gene substitution. Six other clones of the smaller molecules represented the following variants of the SSAV genome: (i) two clones of the entire genome containing only one long terminal repeat unit; (ii) one clone with the 1.85-kb deletion of the pol gene observed in SSSV; and (iii) three clones having a deletion of the 3' end of the SSAV genome. In each of the latter clones, the 5' border of the deletion was indistinguishable from the 5' border of the onc substitution in SSV. The fidelity of genetic deletions observed suggested that certain regions of the SSAV genome were deleted at a high frequency. In certain cases, these deletions may have been accompanied by a substitution of cellular sequences to generate SSV.

摘要

从急性感染猿猴肉瘤病毒(SSV)及其相关辅助病毒(猿猴肉瘤相关病毒[SSAV])的组织培养细胞中分离出染色体外DNA。分离出两种大小的闭环病毒基因组DNA中间体,在单个EcoRI位点切割,然后连接到Charon 21A噬菌体λ载体上。较大尺寸的克隆分子均代表全长(9.0千碱基[kb])的SSAV分子。一组异质克隆源自较小的DNA环。这些包括SSV基因组和SSAV缺失突变体。当将两个SSV克隆与辅助病毒进行比较时,它们包含以下三个特征性缺失:(i)在基因组5'端约1.0 kb处的gag基因中有一个250碱基对的缺失;(ii)pol基因中有一个1.85 kb的缺失;(iii)3'端有一个1.9 kb的缺失,其中包括env基因的一部分。后一个缺失是癌基因替代的位点。其他六个较小分子的克隆代表了SSAV基因组的以下变体:(i)两个仅包含一个长末端重复单元的完整基因组克隆;(ii)一个具有在SSSV中观察到的pol基因1.85 kb缺失的克隆;(iii)三个具有SSAV基因组3'端缺失的克隆。在每个后一种克隆中,缺失的5'边界与SSV中癌基因替代的5'边界无法区分。观察到的基因缺失的保真度表明,SSAV基因组的某些区域被高频缺失。在某些情况下,这些缺失可能伴随着细胞序列的替代以产生SSV。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2439/256788/a41f43cf4f8d/jvirol00161-0252-a.jpg

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