scholarly journals THAP1: Role in Mouse Embryonic Stem Cell Survival and Differentiation

2017 ◽  
Vol 9 (1) ◽  
pp. 92-107 ◽  
Author(s):  
Francesca Aguilo ◽  
Zuchra Zakirova ◽  
Katie Nolan ◽  
Ryan Wagner ◽  
Rajal Sharma ◽  
...  
2019 ◽  
Author(s):  
Aksana Schneider ◽  
Michael Hiller ◽  
Frank Buchholz

Withdrawal statementThe authors have withdrawn their manuscript from bioRxiv regretfully. During additional experiments for the revision we noticed inconsistencies in some results, which may affect the main conclusion of the manuscript. In particular, we noticed that using different primer pairs, some clones that were classified as homozygous knockouts, are actually not knockouts. These were unexpected findings, but might reflect the recently described larger rearrangements observed using CRISPR technology1,2,3,4. Follow up experiments are ongoing, but we would like to withdraw the manuscript at this point in time to avoid misunderstandings. Therefore, the manuscript should currently not be cited. Any questions regarding the manuscript should be addressed to the corresponding author.


2021 ◽  
Author(s):  
Elisabeth Scheer ◽  
Jie Luo ◽  
Frank Ruffenach ◽  
Jean-Marie Garnier ◽  
Isabelle Kolb-Cheynel ◽  
...  

The human general transcription factor TFIID is composed of the TATA-binding protein (TBP) and 13 TBP-associated factors (TAFs). In eukaryotic cells, TFIID is thought to nucleate RNA polymerase II (Pol II) preinitiation complex formation on all protein coding gene promoters and thus, be crucial for Pol II transcription. TFIID is composed of three lobes, named A, B and C. Structural studies showed that TAF8 forms a histone fold pair with TAF10 in lobe B and participates in connecting lobe B to lobe C. In the present study, we have investigated the requirement of the different regions of TAF8 for in vitro TFIID assembly, and the importance of certain TAF8 regions for mouse embryonic stem cell (ESC) viability. We have identified a TAF8 region, different from the histone fold domain of TAF8, important for assembling with the 5TAF core complex in lobe B, and four regions of TAF8 each individually required for interacting with TAF2 in lobe C. Moreover, we show that the 5TAF core-interacting TAF8 domain, and the proline rich domain of TAF8 that interacts with TAF2, are both required for mouse embryonic stem cell survival. Thus, our study demonstrates that distinct TAF8 regions involved in connecting lobe B to lobe C are crucial for TFIID function and consequent ESC survival.


2006 ◽  
Vol 24 (3) ◽  
pp. 344-350 ◽  
Author(s):  
April D Pyle ◽  
Leslie F Lock ◽  
Peter J Donovan

2007 ◽  
Vol 24 (4) ◽  
pp. 625-637 ◽  
Author(s):  
Marek Molcanyi ◽  
Peter Riess ◽  
Kristine Bentz ◽  
Marc Maegele ◽  
Jürgen Hescheler ◽  
...  

2012 ◽  
Vol 23 (18) ◽  
pp. 3754-3763 ◽  
Author(s):  
Li Rong ◽  
Jie Liu ◽  
Yanmei Qi ◽  
Alan M. Graham ◽  
Michael S. Parmacek ◽  
...  

GATA-6 is a zinc-finger transcription factor essential for early embryogenesis. Ablation of GATA-6 in mice impairs endoderm differentiation and causes apoptosis of epiblast cells. The endoderm defects have been attributed to the loss of HNF4, disabled-2, and GATA-4. However, the mechanisms underlying epiblast apoptosis are unclear. In this study we used mouse embryonic stem cell–derived embryoid bodies (EBs) as a model for peri-implantation development and found that ablation of GATA-6 causes massive apoptosis during EB differentiation. Endoderm grafting experiments and ectopic basement membrane (BM) assembly suggest that both BM and non-BM factors contribute to cell survival. Furthermore, the increased cell death in mutant EBs is accompanied by reduced expression of bone morphogenetic protein 2 (BMP-2). Chromatin immunoprecipitation reveals direct binding of GATA-6 to the Bmp2 promoter. Treatment of the mutant EBs with BMP-2 markedly suppresses apoptosis, whereas stable overexpression of the BMP antagonist noggin or a dominant-negative BMP receptor in normal EBs leads to increased apoptosis. Last, activation of SMAD1/5 by phosphorylation is significantly inhibited in the absence of GATA-6, and this is reversed by exogenous BMP-2. Treatment of normal EBs with SMAD phosphorylation inhibitor increases apoptosis. Collectively these results suggest that GATA-6 promotes cell survival by regulating endoderm expression of BMP-2 and BM during embryonic epithelial morphogenesis.


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