BACTERIOPHAGE-LAMBDA N-DEPENDENT TRANSCRIPTION ANTITERMINATION - COMPETITION FOR AN RNA SITE MAY REGULATE ANTITERMINATION
BACTERIOPHAGE-LAMBDA N-DEPENDENT TRANSCRIPTION ANTITERMINATION - COMPETITION FOR AN RNA SITE MAY REGULATE ANTITERMINATION
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DOI：
10.1006/jmbi.1994.1131
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发表时间：
1994-02-11
影响因子：
5.6
通讯作者：
COURT, DL
中科院分区：
文献类型：
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作者：
PATTERSON, TA;ZHANG, ZS;COURT, DL
λ噬菌体通过一系列转录终止和反终止事件以时间方式控制其早期基因的表达。这种抗终止作用需要λ N蛋白以及宿主蛋白Nus和顺式作用位点nut。在utsite转录后，N和Nus蛋白与utRNA结合，并将转录复合物修饰为抗终止形式。该位点是至少两个组分的复合物，一个是与N相互作用的boxB发夹结构。另一个是boxA，boxB上游的9个核苷酸序列。为了进一步了解抗终止复合物的形成，我们研究了boxA基因点突变和缺失对抗终止的影响。发现框A中的点突变增强或减少N-介导的抗终止。另一方面，除了消除对NusB宿主蛋白的需求外，几个boxA缺失对抗终止作用几乎没有影响。为了解释这些观察结果，我们提出，至少有两个因素完成与boxA，NusB和抗终止反应的抑制剂相互作用。此外，我们提出NusB是防止抑制剂结合atboxA所必需的。不同nusBandboxA突变的结果可以用NusB和boxARNA抑制剂之间的竞争模型来解释。
Bacteriophage λ controls the expression of its early genes in a temporal manner by a series of transcription termination and antitermination events. This antitermination requires the λ N protein as well as host proteins called Nus, andcis-acting sites callednut. Following transcription of thenutsite, N and Nus proteins bind to thenutRNA and modify the transcription complex to a termination-resistant form. Thenutsite is a composite of at least two components; one is theboxBhairpin structure which interacts with N. The other isboxA, a nine-nucleotide sequence upstream ofboxB. To understand more about the formation of the antitermination complex, we have characterized the effect of point mutations in and deletions ofboxAon antitermination. Point mutations inboxAwere found to either enhance or reduce N-mediated antitermination. SeveralboxAdeletions, on the other hand, had little effect on antitermination other than to eliminate the requirement for the NusB host protein. To explain these observations, we propose that at least two factors complete to interact withboxA, NusB and an inhibitor of the antitermination reaction. In addition, we propose that NusB is required to prevent the inhibitor from binding atboxA. The results with variousnusBandboxAmutations can be explained by this model of competition between NusB and an inhibitor forboxARNA.