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古菌中病毒转录因子的结构与机制

Structure and mechanisms of viral transcription factors in archaea.

作者信息

Sheppard Carol, Werner Finn

机构信息

Division of Biosciences, Institute of Structural and Molecular Biology, University College London, London, WC1E 6BT, UK.

出版信息

Extremophiles. 2017 Sep;21(5):829-838. doi: 10.1007/s00792-017-0951-1. Epub 2017 Jul 5.

Abstract

Virus-encoded transcription factors have been pivotal in exploring the molecular mechanisms and regulation of gene expression in bacteria and eukaryotes since the birth of molecular biology, while our understanding of viral transcription in archaea is still in its infancy. Archaeal viruses do not encode their own RNA polymerases (RNAPs) and are consequently entirely dependent on their hosts for gene expression; this is fundamentally different from many bacteriophages and requires alternative regulatory strategies. Archaeal viruses wield a repertoire of proteins to expropriate the host transcription machinery to their own benefit. In this short review we summarise our current understanding of gene-specific and global mechanisms that viruses employ to chiefly downregulate host transcription and enable the efficient and temporal expression of the viral transcriptome. Most of the experimentally characterised archaeo-viral transcription regulators possess either ribbon-helix-helix or Zn-finger motifs that allow them to engage with the DNA in a sequence-specific manner, altering the expression of a specific subset of genes. Recently a novel type of regulator was reported that directly binds to the RNAP and shuts down transcription of both host and viral genes in a global fashion.

摘要

自分子生物学诞生以来,病毒编码的转录因子在探索细菌和真核生物基因表达的分子机制及调控方面发挥了关键作用,而我们对古菌中病毒转录的理解仍处于起步阶段。古菌病毒不编码自身的RNA聚合酶(RNAP),因此其基因表达完全依赖宿主;这与许多噬菌体有根本区别,需要不同的调控策略。古菌病毒利用一系列蛋白质来为自身利益征用宿主转录机制。在这篇简短的综述中,我们总结了目前对病毒主要用于下调宿主转录并实现病毒转录组高效和适时表达的基因特异性和全局机制的理解。大多数经过实验表征的古菌病毒转录调节因子具有带状螺旋-螺旋或锌指基序,使它们能够以序列特异性方式与DNA结合,改变特定基因子集的表达。最近报道了一种新型调节因子,它直接与RNAP结合并以全局方式关闭宿主和病毒基因的转录。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/def2/5569661/e05f744cef04/792_2017_951_Fig1_HTML.jpg

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