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TAF4是转录因子IID的一个亚基，在出生后肝细胞分化过程中指导核受体HNF4A对启动子的占据。

TAF4, a subunit of transcription factor II D, directs promoter occupancy of nuclear receptor HNF4A during post-natal hepatocyte differentiation.

作者信息

Alpern Daniil, Langer Diana, Ballester Benoit, Le Gras Stephanie, Romier Christophe, Mengus Gabrielle, Davidson Irwin

机构信息

Department of Functional Genomics and Cancer, Institut de Genetique et de Biologie Moleculaire et Cellulaire, CNRS/INSERM/UDS, Illkirch, France.

Laboratoire TAGC, Aix-Marseille Université, UMR1090, Marseille, France.

出版信息

Elife. 2014 Sep 10;3:e03613. doi: 10.7554/eLife.03613.

DOI:10.7554/eLife.03613
PMID:25209997
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4359380/
Abstract

The functions of the TAF subunits of mammalian TFIID in physiological processes remain poorly characterised. In this study, we describe a novel function of TAFs in directing genomic occupancy of a transcriptional activator. Using liver-specific inactivation in mice, we show that the TAF4 subunit of TFIID is required for post-natal hepatocyte maturation. TAF4 promotes pre-initiation complex (PIC) formation at post-natal expressed liver function genes and down-regulates a subset of embryonic expressed genes by increased RNA polymerase II pausing. The TAF4-TAF12 heterodimer interacts directly with HNF4A and in vivo TAF4 is necessary to maintain HNF4A-directed embryonic gene expression at post-natal stages and promotes HNF4A occupancy of functional cis-regulatory elements adjacent to the transcription start sites of post-natal expressed genes. Stable HNF4A occupancy of these regulatory elements requires TAF4-dependent PIC formation highlighting that these are mutually dependent events. Local promoter-proximal HNF4A-TFIID interactions therefore act as instructive signals for post-natal hepatocyte differentiation.

摘要

哺乳动物TFIID的TAF亚基在生理过程中的功能仍未得到充分表征。在本研究中，我们描述了TAF在指导转录激活因子的基因组占据方面的新功能。利用小鼠肝脏特异性失活，我们表明TFIID的TAF4亚基是出生后肝细胞成熟所必需的。TAF4促进出生后表达的肝功能基因处的预起始复合物（PIC）形成，并通过增加RNA聚合酶II的暂停来下调一部分胚胎表达基因。TAF4-TAF12异二聚体直接与HNF4A相互作用，并且在体内，TAF4对于在出生后阶段维持HNF4A指导的胚胎基因表达是必需的，并且促进HNF4A占据出生后表达基因转录起始位点附近的功能性顺式调节元件。这些调节元件的稳定HNF4A占据需要TAF4依赖的PIC形成，突出表明这些是相互依赖的事件。因此，局部启动子近端的HNF4A-TFIID相互作用作为出生后肝细胞分化的指导信号。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/74ae4446cb44/elife03613f009.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/b563298c33bf/elife03613fs006.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/25ca1fa9efb0/elife03613f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/7bad94225cbb/elife03613fs001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/d2bcc35f4d66/elife03613f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/82e552842df4/elife03613fs002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/8bb7836c8a26/elife03613f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/325951c273dd/elife03613fs003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/89c7b6488477/elife03613f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/bc352393e168/elife03613fs004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/890789b7e212/elife03613f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/7408b2a79e42/elife03613f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/4222aa81ac0d/elife03613fs005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/d474abe376ee/elife03613f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/6e90bd35fc03/elife03613f008.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/77301e7136e9/elife03613fs007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0198/4359380/74ae4446cb44/elife03613f009.jpg

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