Altered subcellular localization of transcription factor TEAD4 regulates first mammalian cell lineage commitment

Pratik Home; Biswarup Saha; Soma Ray; Debasree Dutta; Sumedha Gunewardena; Byunggil Yoo; Arindam Pal; Jay L. Vivian; Melissa Larson; Margaret Petroff; Patrick G. Gallagher; Vincent P. Schulz; Kenneth L. White; Thaddeus G. Golos; Barry Behr; Soumen Paul

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Altered subcellular localization of transcription factor TEAD4 regulates first mammalian cell lineage commitment

机译：转录因子TEAD4的亚细胞定位改变可调节第一个哺乳动物细胞谱系承诺

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In the preimplantation mouse embryo, TEAD4 is critical to establishing the trophectoderm (TE)-specific transcriptional program and segregating TE from the inner cell mass (ICM). However, TEAD4 is expressed in the TE and the ICM. Thus, differential function of TEAD4 rather than expression itself regulates specification of the first two cell lineages. We used ChIP sequencing to define genomewide TEAD4 target genes and asked how transcription of TEAD4 target genes is specifically maintained in the TE. Our analyses revealed an evolutionary conserved mechanism, in which lack of nuclear localization of TEAD4 impairs the TE-specific transcriptional program in inner blastomeres, thereby allowing their maturation toward the ICM lineage. Restoration of TEAD4 nucjear localization maintains the TE-specific transcriptional program in the inner blastomeres and prevents segregation of the TE and ICM lineages and blastocyst formation. We propose that altered subcellular localization of TEAD4 in blastomeres dictates first mammalian cell fate specification.

机译：在植入前的小鼠胚胎中，TEAD4对于建立滋养外胚层（TE）特异性转录程序以及将TE与内部细胞团（ICM）隔离至关重要。但是，TEAD4在TE和ICM中表示。因此，TEAD4的差异功能而不是表达本身调节前两个细胞谱系的规格。我们使用ChIP测序来定义全基因组的TEAD4靶基因，并询问TEAD4靶基因的转录如何在TE中特异性维持。我们的分析揭示了一种进化的保守机制，其中TEAD4的核定位不足会破坏内部卵裂球中的TE特异性转录程序，从而使其向ICM谱系成熟。 TEAD4核素定位的恢复在内部卵裂球中维持TE特异性转录程序，并防止TE和ICM谱系分离和胚泡形成。我们建议改变卵裂球中的TEAD4的亚细胞定位决定了第一个哺乳动物细胞的命运规范。

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《Proceedings of the National Academy of Sciences of the United States of America》 |2012年第19期|p.7362-7367|共6页
作者
Pratik Home; Biswarup Saha; Soma Ray; Debasree Dutta; Sumedha Gunewardena; Byunggil Yoo; Arindam Pal; Jay L. Vivian; Melissa Larson; Margaret Petroff; Patrick G. Gallagher; Vincent P. Schulz; Kenneth L. White; Thaddeus G. Golos; Barry Behr; Soumen Paul;
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作者单位

Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160;

Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160;

Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160;

Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160;

Smith Intellectual Developmental Disabilities Research Center, University of Kansas Medical Center, Kansas City, KS 66160;

Smith Intellectual Developmental Disabilities Research Center, University of Kansas Medical Center, Kansas City, KS 66160;

Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160,Institute of Reproductive Health and Regenerative Medicine, and Departments of University of Kansas Medical Center, Kansas City, KS 66160;

Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160,Institute of Reproductive Health and Regenerative Medicine, and Departments of University of Kansas Medical Center, Kansas City, KS 66160;

Physiology , University of Kansas Medical Center, Kansas City, KS 66160;

Anatomy and Cell Biology, University of Kansas Medical Center, Kansas City, KS 66160;

Department of Pediatrics, Yale University School of Medicine, New Haven, CT 06510;

Department of Pediatrics, Yale University School of Medicine, New Haven, CT 06510;

Animal, Dairy and Veterinary Sciences Department, Utah State University, Logan, UT 84322;

Departments of Comparative Biosciences and Obstetrics and Gynecology, University of Wisconsin, Madison, Wl 53715;

Department of Gynecology and Obstetrics, Stanford University School of Medicine, Stanford, CA 94305;

Department of Pathology and Laboratory Medicine, University of Kansas Medical Center, Kansas City, KS 66160,Institute of Reproductive Health and Regenerative Medicine, and Departments of University of Kansas Medical Center, Kansas City, KS 66160;

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收录信息美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
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1. Transcription factor TEAD4 specifies the trophectoderm lineage at the beginning of mammalian development. [J] . Yagi R, Kohn MJ, Karavanova I, Development . 2007,第21期

机译：转录因子TEAD4在哺乳动物发育开始时指定了滋养外胚层谱系。
2. Novel Basic Helix-Loop-Helix Transcription Factor Hes4 Antagonizes the Function of Twist-1 to Regulate Lineage Commitment of Bone Marrow Stromal/Stem Cells [J] . Cakouros Dimitrios, Isenmann Sandra, Hemming Sarah Elizabeth, Stem cells and development . 2015,第11期

机译：新型基本螺旋环转录因子Hes4拮抗Twist-1调节骨髓基质/干细胞谱系承诺的功能。
3. Mitochondria-to-nuclear signaling is regulated by the subcellular localization of the transcription factors Rtg1p and Rtg3p [J] . Sekito T., Butow RA., Thornton J. Molecular biology of the cell . 2000,第6期

机译：线粒体到核信号转导受转录因子Rtg1p和Rtg3p的亚细胞定位
4. Discovery of Transcription Factors Using Protein Subcellular Localization Prediction and Gene Expression Profile Analysis [C] . Amitava Karmaker, Mark Doderer, Stephen E. Harris, International Conference on Machine Learning . 2007

机译：使用蛋白质亚细胞定位预测和基因表达分析分析的转录因子发现
5. Identification of an E2A-regulated transcriptional network controlling T lineage commitment and transformation. [D] . Xu, Wei. 2010

机译：鉴定E2A调控的转录网络，控制T谱系的定型和转化。
6. Altered subcellular localization of transcription factor TEAD4 regulates first mammalian cell lineage commitment [O] . Pratik Home, Biswarup Saha, Soma Ray, 2012

机译：转录因子TEAD4的亚细胞定位改变可调节第一个哺乳动物细胞谱系承诺
7. Altered subcellular localization of transcription factor TEAD4 regulates first mammalian cell lineage commitment [O] . Home, Pratik, Saha, Biswarup, Ray, Soma, 2012

机译：转录因子TEAD4的亚细胞定位改变可调节第一个哺乳动物细胞谱系承诺

Altered subcellular localization of transcription factor TEAD4 regulates first mammalian cell lineage commitment

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