Incomplete splicing and deficient accumulation of the fiber messenger RNA in monkey cells infected by human adenovirus type 2.
Incomplete splicing and deficient accumulation of the fiber messenger RNA in monkey cells infected by human adenovirus type 2.
复制标题
被人 2 型腺病毒感染的猴细胞中纤维信使 RNA 的剪接不完全和积累不足。
DOI：
10.1016/0022-2836(80)90306-x
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发表时间：
1980
影响因子：
5.6
通讯作者：
L. Chow
中科院分区：
文献类型：
--
作者：
D. Klessig;L. Chow
猴细胞是人类腺病毒的不允许宿主，因为某些晚期病毒蛋白的合成受阻。对流产感染的猴细胞产生的RNA的分析表明，许多晚期蛋白质的合成受到抑制可以归因于它们相应的mRNAs浓度的降低(Klessig&Anderson，1975)。衣壳多肽纤维是个例外。猴子细胞中纤维RNA的浓度降低了5到20倍，而纤维蛋白质的合成则被抑制了100到1000倍。为检测细胞质纤维RNA中的缺陷而设计的实验表明，RNA的5‘末端有一个正常的、有帽的三方先导。然而，这些分子中有很大一部分含有三方前导和主体之间的长序列，在纤维mRNA的成熟过程中，这些序列未能从最初的转录本中剪接出来。类似地，在晚期，区域3的RNA在流产感染中也包含相同的长上游序列。相比之下，在猴子细胞中裂解生长的2型腺病毒突变体的生产性感染所产生的细胞质纤维或区域3 RNA很少保留如此长的上游序列。其他来自流产或高效感染的猴子细胞的晚期RNA具有与允许的人类细胞相同的剪接模式。这些观察表明，RNA剪接在基因表达控制中发挥了作用，并可能代表了由于RNA剪接缺陷而导致的病毒宿主范围有限的一个例子。
Monkey cells are non-permissive hosts for human adenoviruses due to a block in the synthesis of certain late viral proteins. Analysis of the RNA produced in abortively infected monkey cells indicated that the depressed synthesis of many of the late proteins can be ascribed to the reduced concentration of their corresponding mRNAs (Klessig & Anderson, 1975). An exception is the capsid polypeptide, fiber. Fiber RNA concentration is reduced by five- to 20-fold in monkey cells, whereas fiber protein synthesis is depressed by 100 to 1000-fold. Experiments designed to detect defects in the cytoplasmic fiber RNA which would account for its poor translatability showed that the RNA had a normal, capped tripartite leader at its 5′ terminus. However, a large proportion of these molecules contained long sequences between the tripartite leader and the main body which failed to be spliced out of the initial transcript during maturation of the fiber mRNA. Similarly, region 3 RNAs at late times also contained the same long upstream sequences in abortive infections. In contrast, few cytoplasmic fiber or region 3 RNAs from a productive infection with an adenovirus type 2 mutant, which grows lytically in monkey cells, retained such long upstream sequences. The other late RNAs from abortively or productively infected monkey cells had splicing patterns identical to those seen in permissive human cells. These observations suggest a role for RNA splicing in the control of gene expression and may represent an example of limited host range of a virus due to deficient RNA splicing.