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微小P1质粒复制:自我调节-隔离悖论

Mini-P1 plasmid replication: the autoregulation-sequestration paradox.

作者信息

Chattoraj D K, Mason R J, Wickner S H

机构信息

Laboratory of Biochemistry, National Cancer Institute, Bethesda, Maryland 20892.

出版信息

Cell. 1988 Feb 26;52(4):551-7. doi: 10.1016/0092-8674(88)90468-0.

Abstract

It has been proposed that the initiator protein RepA is rate limiting for mini-P1 plasmid replication, and that the role of the plasmid copy number control locus is to sequester the initiator and thus reduce replication. This proposal appears inconsistent with the observation that RepA is autoregulated, since the protein lost by sequestration should be replenished. A resolution of this autoregulation-sequestration paradox is possible if the sequestered RepA, unavailable for replication, is still available for promoter repression. We demonstrate that RepA binds to the control locus and to the promoter region simultaneously, causing the intervening DNA to loop. DNA looping could provide the requisite mechanism by which RepA bound to the control locus might exert repression.

摘要

有人提出起始蛋白RepA是mini - P1质粒复制的限速因素,并且质粒拷贝数控制位点的作用是隔离起始蛋白从而减少复制。这一观点似乎与RepA受到自身调控的观察结果不一致,因为被隔离而损失的蛋白质应该得到补充。如果被隔离的、无法用于复制的RepA仍可用于启动子抑制,那么就有可能解决这种自身调控 - 隔离的矛盾。我们证明RepA同时与控制位点和启动子区域结合,使中间的DNA形成环。DNA环化可能提供了一种必要的机制,通过这种机制,结合在控制位点的RepA可能发挥抑制作用。

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