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转录起始位点下游CCAAT/增强子结合蛋白位点的功能研究

Functional Studies of CCAAT/Enhancer Binding Protein Site Located Downstream of the Transcriptional Start Site.

作者信息

Liu Yujie, Nonnemacher Michael R, Alexaki Aikaterini, Pirrone Vanessa, Banerjee Anupam, Li Luna, Kilareski Evelyn, Wigdahl Brian

机构信息

Department of Microbiology and Immunology, Center for Molecular Virology and Translational Neuroscience, Institute for Molecular Medicine and Infectious Disease, Drexel University College of Medicine, Philadelphia, PA, USA.

Sidney Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA.

出版信息

Clin Med Insights Pathol. 2017 Nov 15;10:1179555717694556. doi: 10.1177/1179555717694556. eCollection 2017.

DOI:10.1177/1179555717694556
PMID:29162980
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5692137/
Abstract

Previous studies have identified a CCAAT/enhancer binding protein (C/EBP) site located downstream of the transcriptional start site (DS3). The role of the DS3 element with respect to HIV-1 transactivation by Tat and viral replication has not been characterized. We have demonstrated that DS3 was a functional C/EBPβ binding site and mutation of this site to the C/EBP knockout DS3-9C variant showed lower HIV-1 long terminal repeat (LTR) transactivation by C/EBPβ. However, it was able to exhibit similar or even higher transcription levels by Tat compared to the parental LTR. C/EBPβ and Tat together further enhanced the transcription level of the parental LAI-LTR and DS3-9C LTR, with higher levels in the DS3-9C LTR. HIV molecular clone viruses carrying the DS3-9C variant LTR demonstrated a decreased replication capacity and delayed rate of replication. These results suggest that DS3 plays a role in virus transcriptional initiation and provides new insight into C/EBP regulation of HIV-1.

摘要

先前的研究已经确定了一个位于转录起始位点（DS3）下游的CCAAT/增强子结合蛋白（C/EBP）位点。关于DS3元件在Tat介导的HIV-1反式激活及病毒复制方面的作用尚未得到明确阐述。我们已经证明DS3是一个功能性的C/EBPβ结合位点，将该位点突变为C/EBP基因敲除的DS3-9C变体后，C/EBPβ对HIV-1长末端重复序列（LTR）的反式激活作用降低。然而，与亲本LTR相比，它在Tat作用下能够表现出相似甚至更高的转录水平。C/EBPβ和Tat共同作用进一步增强了亲本LAI-LTR和DS3-9C LTR的转录水平，其中DS3-9C LTR的水平更高。携带DS3-9C变体LTR的HIV分子克隆病毒表现出复制能力下降和复制速率延迟。这些结果表明DS3在病毒转录起始中发挥作用，并为C/EBP对HIV-1的调控提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00f1/5692137/e1ea170f1f83/10.1177_1179555717694556-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00f1/5692137/54cd0a87ddf6/10.1177_1179555717694556-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00f1/5692137/7071ce8f3ef2/10.1177_1179555717694556-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00f1/5692137/d214d4cd1e9d/10.1177_1179555717694556-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00f1/5692137/f10fa51392bc/10.1177_1179555717694556-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00f1/5692137/e1ea170f1f83/10.1177_1179555717694556-fig5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00f1/5692137/54cd0a87ddf6/10.1177_1179555717694556-fig1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00f1/5692137/7071ce8f3ef2/10.1177_1179555717694556-fig2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00f1/5692137/d214d4cd1e9d/10.1177_1179555717694556-fig3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00f1/5692137/f10fa51392bc/10.1177_1179555717694556-fig4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/00f1/5692137/e1ea170f1f83/10.1177_1179555717694556-fig5.jpg

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