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[含RNA噬菌体中RNA复制的调控。衣壳蛋白极性突变体中的RNA合成]

[Regulation of RNA replication in RNA-containing bacteriphages. RNA synthesis in coat protein polar mutants].

作者信息

Pumpen P P, Bauman V R, Dishler A V, Gren E Ia

出版信息

Genetika. 1978 Oct;14(10):1687-95.

PMID:363501
Abstract

The synthesis of RNA by polar coat protein mutants f2sus3 and Qbetaam12 under suppressor (Escherichia coli S26R1E, Su+-1; H12R8a Su+-3) and non-suppressor (E. coli AB259; S26) conditions was examined. It was demonstrated that the synthesis of viral RNA under non-suppressor conditions in the presence of rifamycin produced the same gaussian pattern of rates as the synthesis of RNA by wild type phage or non-polar coat protein mutants. However, the total amount of RNA was decreased approximately 10-fold and the peak of RNA synthesis was displaced 7--10 min later. The number of infective centers was reduced also 10-fold indicating that a certain time-lapse was required to overcome the polarity of the parental RNA, this process being of single occurrence, exclusively on the parental RNA, but not on the progeny strains. As a consequence, it was concluded that the initiation of translation at the replicase cistron starts on the nascent RNA chains within the replicative complexes and not on the fully-synthesized templates with their complete secondary structure. The data obtained are not in contradiction with the hypothesis concerning the role of the repressor complex II (replicase-RNA) to slow down the synthesis of replicase and RNA in the coat protein mutants. The polarity can not be responsible probably for the blocking of the replicase cistron on the nascent chain following the block of coat protein cistron. Therefore, it appears appropriate to assume the existence of two binding sites for the replicase as repressor which is in keeping with the conclusions of Weissmann and co-workers.

摘要

在抑制条件(大肠杆菌S26R1E,Su + -1;H12R8a Su + -3)和非抑制条件(大肠杆菌AB259;S26)下,研究了极性外壳蛋白突变体f2sus3和Qβam12合成RNA的情况。结果表明,在非抑制条件下,利福平存在时病毒RNA的合成产生了与野生型噬菌体或非极性外壳蛋白突变体合成RNA相同的高斯速率模式。然而,RNA的总量大约减少了10倍,RNA合成的峰值推迟了7 - 10分钟出现。感染中心的数量也减少了10倍,这表明需要一定的时间间隔来克服亲本RNA的极性,这个过程只发生在亲本RNA上,而不在子代菌株上。因此,可以得出结论,复制酶顺反子处的翻译起始是在复制复合物中的新生RNA链上开始的,而不是在具有完整二级结构的完全合成模板上开始。所获得的数据与关于阻遏复合物II(复制酶 - RNA)在外壳蛋白突变体中减缓复制酶和RNA合成作用的假设并不矛盾。极性可能不是在外壳蛋白顺反子被阻断后导致新生链上复制酶顺反子被阻断的原因。因此,似乎有理由假设存在两个作为阻遏物的复制酶结合位点,这与魏斯曼及其同事的结论一致。

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