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T4 晚期基因的转录。

Transcription of the T4 late genes.

机构信息

Division of Biological Sciences, Section of Molecular Biology, University of California, San Diego, La Jolla, CA 92093-0634, USA.

出版信息

Virol J. 2010 Oct 28;7:288. doi: 10.1186/1743-422X-7-288.

DOI:10.1186/1743-422X-7-288
PMID:21029432
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2988020/
Abstract

This article reviews the current state of understanding of the regulated transcription of the bacteriophage T4 late genes, with a focus on the underlying biochemical mechanisms, which turn out to be unique to the T4-related family of phages or significantly different from other bacterial systems. The activator of T4 late transcription is the gene 45 protein (gp45), the sliding clamp of the T4 replisome. Gp45 becomes topologically linked to DNA through the action of its clamp-loader, but it is not site-specifically DNA-bound, as other transcriptional activators are. Gp45 facilitates RNA polymerase recruitment to late promoters by interacting with two phage-encoded polymerase subunits: gp33, the co-activator of T4 late transcription; and gp55, the T4 late promoter recognition protein. The emphasis of this account is on the sites and mechanisms of actions of these three proteins, and on their roles in the formation of transcription-ready open T4 late promoter complexes.

摘要

本文综述了目前对噬菌体 T4 晚期基因的调控转录的理解,重点介绍了潜在的生化机制,这些机制对于 T4 相关噬菌体家族来说是独特的,或者与其他细菌系统有很大的不同。T4 晚期转录的激活剂是基因 45 蛋白(gp45),即 T4 复制体的滑动夹。gp45 通过其夹载器的作用与 DNA 拓扑连接,但它不像其他转录激活剂那样与 DNA 特异性结合。gp45 通过与两种噬菌体编码的聚合酶亚基相互作用,促进 RNA 聚合酶募集到晚期启动子:gp33,T4 晚期转录的共激活因子;和 gp55,T4 晚期启动子识别蛋白。本文的重点是这三种蛋白质的作用位点和作用机制,以及它们在形成转录准备好的开放 T4 晚期启动子复合物中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b8/2988020/d808d51c88a4/1743-422X-7-288-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b8/2988020/a355b7a800b7/1743-422X-7-288-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b8/2988020/8f2d4990a931/1743-422X-7-288-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b8/2988020/8655a7f611ec/1743-422X-7-288-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b8/2988020/a4d3546e66aa/1743-422X-7-288-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b8/2988020/c3310c58aed1/1743-422X-7-288-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b8/2988020/d808d51c88a4/1743-422X-7-288-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b8/2988020/a355b7a800b7/1743-422X-7-288-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b8/2988020/8f2d4990a931/1743-422X-7-288-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b8/2988020/8655a7f611ec/1743-422X-7-288-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b8/2988020/a4d3546e66aa/1743-422X-7-288-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b8/2988020/c3310c58aed1/1743-422X-7-288-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b2b8/2988020/d808d51c88a4/1743-422X-7-288-6.jpg

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Virol J. 2010 Oct 28;7:292. doi: 10.1186/1743-422X-7-292.
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Nat Microbiol. 2025 Feb;10(2):448-467. doi: 10.1038/s41564-024-01915-3. Epub 2025 Jan 23.
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