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抑制感染水疱性口炎病毒的小鼠L细胞中核糖核酸的积累需要病毒核糖核酸转录。

Inhibition of ribonucleic acid accumulation in mouse L cells infected with vesicular stomatitis virus requires viral ribonucleic acid transcription.

作者信息

Wu F S, Lucas-Lenard J M

出版信息

Biochemistry. 1980 Feb 19;19(4):804-10. doi: 10.1021/bi00545a029.

Abstract

The accumulation of ribonucleic acid (RNA) in mouse L-929 cells infected with temperature-sensitive mutants of vesicular stomatitis virus or ultraviolet- (UV-) irradiated virus was studied. At the permissive temperature (30 degrees C infection by all mutants resulted in an inhibition of cellular RNA accumulation. At the nonpermissive temperature (40 degrees C) mutants G114 (I) and G22 (II) failed to inhibit RNA accumulation, but mutants G11 (I), O52 (II), G31 (III), G33 (III), G41 (IV), W10 (IV), O45 (V), and O110 (V) were still active in this respect. In most cases the accumulation of 28S and 18S mature rRNA was inhibited to a greater extent than the synthesis of the 45S rRNA precursor. UV irradiation of wild type virus considerably reduced its capacity to inhibit cellular RNA synthesis. The target size for inactivation of this capacity of the virus was approximately 17% of the viral genome or that corresponding to the N gene. These results indicate that the virion proteins themselves are incapable of inhibiting cellular RNA synthesis and that transcription of approximately 17% of the genome is required. Expression of RNA synthesis inhibition also requires some function of virion NS protein in addition to its transcriptase activity.

摘要

研究了感染水疱性口炎病毒温度敏感突变体或紫外线(UV)照射病毒的小鼠L - 929细胞中核糖核酸(RNA)的积累情况。在允许温度(30℃)下,所有突变体感染均导致细胞RNA积累受到抑制。在非允许温度(40℃)下,突变体G114(I)和G22(II)未能抑制RNA积累,但突变体G11(I)、O52(II)、G31(III)、G33(III)、G41(IV)、W10(IV)、O45(V)和O110(V)在这方面仍具有活性。在大多数情况下,28S和18S成熟rRNA的积累比45S rRNA前体的合成受到更大程度的抑制。野生型病毒经紫外线照射后,其抑制细胞RNA合成的能力大大降低。使病毒这种能力失活的靶标大小约为病毒基因组的17%或相当于N基因的部分。这些结果表明,病毒粒子蛋白本身无法抑制细胞RNA合成,并且需要约17%的基因组进行转录。RNA合成抑制的表达除了需要病毒粒子NS蛋白的转录酶活性外,还需要其一些功能。

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