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水泡性口炎病毒内部缺失突变体对异常糖蛋白mRNA的条件性合成。

Conditional synthesis of an aberrant glycoprotein mRNA by the internal deletion mutant of vesicular stomatitis virus.

作者信息

Herman R C

出版信息

J Virol. 1983 Jun;46(3):709-17. doi: 10.1128/JVI.46.3.709-717.1983.

Abstract

The internal deletion mutant (DI-LT) derived from the heat-resistant strain of vesicular stomatitis virus synthesizes an aberrant polyadenylated mRNA (G*) containing a transcript of the partially deleted polymerase gene covalently linked to the 3' end of the glycoprotein message (R. C. Herman and R. A. Lazzarini, J. Virol. 40:78-86, 1981). The heat-resistant polymerase appears to play a role in the synthesis of the abnormal G* RNA. The synthesis of G* correlated directly with the presence of the heat-resistant L protein on the defective interfering particle template. Chimeric defective interfering particles produced by passaging DI-LT with a helper virus that encodes the wild-type vesicular stomatitis virus polymerase did not synthesize G*. The subsequent passage of the chimeric DI-LT with a heat-resistant helper virus restored the ability to synthesize the G* transcript. These results imply that the regulatory signals normally present at the vesicular stomatitis virus G/L intercistronic boundary may be preserved in DI-LT. These sequences are only conditionally functional because they are recognized correctly by the wild-type but not by the heat-resistant polymerase.

摘要

源自水疱性口炎病毒耐热株的内部缺失突变体(DI-LT)合成了一种异常的多聚腺苷酸化mRNA(G*),该mRNA包含部分缺失的聚合酶基因的转录本,其与糖蛋白信息的3'端共价连接(R.C.赫尔曼和R.A.拉扎里尼,《病毒学杂志》40:78-86,1981)。耐热聚合酶似乎在异常G* RNA的合成中起作用。G的合成与缺陷干扰颗粒模板上耐热L蛋白的存在直接相关。通过将DI-LT与编码野生型水疱性口炎病毒聚合酶的辅助病毒传代产生的嵌合缺陷干扰颗粒不合成G。随后将嵌合DI-LT与耐热辅助病毒传代恢复了合成G*转录本的能力。这些结果表明,通常存在于水疱性口炎病毒G/L顺反子间边界的调控信号可能在DI-LT中得以保留。这些序列仅具有条件性功能,因为它们能被野生型正确识别,但不能被耐热聚合酶识别。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a604/256547/630119008415/jvirol00147-0041-a.jpg

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