scholarly journals Derivation of extraembryonic endoderm stem (XEN) cells from mouse embryos and embryonic stem cells

2013 ◽  
Vol 8 (6) ◽  
pp. 1028-1041 ◽  
Author(s):  
Kathy K Niakan ◽  
Nadine Schrode ◽  
Lily T Y Cho ◽  
Anna-Katerina Hadjantonakis
2006 ◽  
Vol 74 (4) ◽  
pp. 160-166 ◽  
Author(s):  
Shiro Iuchi ◽  
Meytha Marsch-Moreno ◽  
Cristina Velez-DelValle ◽  
Karen Easley ◽  
Walid Kuri-Harcuch ◽  
...  

Cell Research ◽  
2017 ◽  
Vol 28 (1) ◽  
pp. 126-129 ◽  
Author(s):  
Xuepeng Wang ◽  
Tianda Li ◽  
Tongtong Cui ◽  
Dawei Yu ◽  
Chao Liu ◽  
...  

2011 ◽  
Vol 7 (1) ◽  
pp. 28-40 ◽  
Author(s):  
Calvin Simerly ◽  
Dave McFarland ◽  
Carlos Castro ◽  
Chih-Cheng Lin ◽  
Carrie Redinger ◽  
...  

Nature ◽  
2011 ◽  
Vol 479 (7371) ◽  
pp. 131-134 ◽  
Author(s):  
Martin Leeb ◽  
Anton Wutz

2008 ◽  
Vol 40 (7) ◽  
pp. 921-926 ◽  
Author(s):  
Chi-Wei Lu ◽  
Akiko Yabuuchi ◽  
Lingyi Chen ◽  
Srinivas Viswanathan ◽  
Kitai Kim ◽  
...  

2004 ◽  
Vol 24 (15) ◽  
pp. 6710-6718 ◽  
Author(s):  
Mirei Murakami ◽  
Tomoko Ichisaka ◽  
Mitsuyo Maeda ◽  
Noriko Oshiro ◽  
Kenta Hara ◽  
...  

ABSTRACT TOR is a serine-threonine kinase that was originally identified as a target of rapamycin in Saccharomyces cerevisiae and then found to be highly conserved among eukaryotes. In Drosophila melanogaster, inactivation of TOR or its substrate, S6 kinase, results in reduced cell size and embryonic lethality, indicating a critical role for the TOR pathway in cell growth control. However, the in vivo functions of mammalian TOR (mTOR) remain unclear. In this study, we disrupted the kinase domain of mouse mTOR by homologous recombination. While heterozygous mutant mice were normal and fertile, homozygous mutant embryos died shortly after implantation due to impaired cell proliferation in both embryonic and extraembryonic compartments. Homozygous blastocysts looked normal, but their inner cell mass and trophoblast failed to proliferate in vitro. Deletion of the C-terminal six amino acids of mTOR, which are essential for kinase activity, resulted in reduced cell size and proliferation arrest in embryonic stem cells. These data show that mTOR controls both cell size and proliferation in early mouse embryos and embryonic stem cells.


Stem Cells ◽  
2012 ◽  
Vol 30 (3) ◽  
pp. 461-470 ◽  
Author(s):  
Xuezhu Feng ◽  
Jiuchun Zhang ◽  
Kimberly Smuga-Otto ◽  
Shulan Tian ◽  
Junying Yu ◽  
...  

2007 ◽  
Vol 19 (1) ◽  
pp. 252
Author(s):  
A. Meece ◽  
S. He ◽  
C. Keefer

Lymphoid enhancer-binding factor 1 (Lef1) is a key transcriptional factor in the Wnt signaling pathway. Recently, the Wnt pathway has been shown to function in human and mouse embryonic stem cells; however, its role in ES cell differentiation and self-renewal remains contradictory. Our lab has identified two novel Lef1 isoforms, Lef1Δ2,3,6 and Lef1Δ6, that are transcribed in mouse embryonic stem cells in addition to the full-length Lef1. Both Lef1Δ2,3,6 and Lef1Δ6 contain an N-terminal β-catenin binding domain and a C-terminal HMG DNA binding domain. However, Lef1Δ2,3,6 lacks exons II, III, and VI, and Lef1Δ6 lacks exon VI. Exons II, III, and VI are a part of the context-dependent repression domain, whereas exon VI contains a Groucho binding motif. The absence of these repression domains suggests that Lef1Δ2,3,6 and Lef1Δ6 may be regulated differently than the full-length Lef1. In this study, we determined the expression patterns of Lef1 mRNA and the two isoforms during murine and bovine pre-implantation development using RT-PCR. Total RNA was isolated from pools of 10–20 in vitro-produced bovine embryos at the 2-cell, 4–8 cell, morulae, and blastocyst stages and in vivo-derived mouse embryos at the 8-cell, morula, and blastocyst stages using a Stratagene Nanoprep kit. Reverse transcription was performed using the Invitrogen Supercript III first-strand synthesis system. PCR was then completed using Invitrogen Platinum Taq DNA Polymerase. As determined in preliminary work, full-length Lef1 was expressed in 8-cell-stage mouse embryos but was not detectable in morulae and was only slightly expressed in mouse blastocysts. In contrast, Lef1Δ6 mRNA was not detectable in 8-cell mouse embryos, but became obvious at morula and blastocyst stages. Similarly, in bovine embryos, full-length Lef1 was detected at early cleavage stages (2–8 cells) with undetectable or low levels at the morula and blastocyst stages; however, unlike what was observed in the mouse embryos, Lef1Δ6 was expressed in all stages of bovine embryos tested. Lef1Δ2,3,6 was very low (mouse) or undetected (bovine). Because Lef1 appears to be playing a critical role in response to Wnt differentiation signals in mouse embryonic stem cells (He, unpublished), further exploration of these transcription factors and their regulation in developing mammalian embryos is critical to understanding the process of initial embryonic differentiation.


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