scholarly journals FGF-regulated BMP signaling is required for eyelid closure and to specify conjunctival epithelial cell fate

Development ◽  
2009 ◽  
Vol 136 (10) ◽  
pp. 1741-1750 ◽  
Author(s):  
J. Huang ◽  
L. K. Dattilo ◽  
R. Rajagopal ◽  
Y. Liu ◽  
V. Kaartinen ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Fate ◽  
Bmp Signaling ◽  
Eyelid Closure ◽  
Conjunctival Epithelial Cell

Epidermal induction and inhibition of neural fate by translation initiation factor 4AIII

Development ◽  
1997 ◽  
Vol 124 (21) ◽  
pp. 4235-4242
Author(s):  
D.C. Weinstein ◽  
E. Honore ◽  
A. Hemmati-Brivanlou
Keyword(s):  
Cell Fate ◽  
Translation Initiation ◽  
Mrna Translation ◽  
Bmp Signaling ◽  
Translation Initiation Factor ◽  
Initiation Factor ◽  
Neural Fate ◽  
Morphogenetic Protein ◽  
Dissociated Cells ◽  
A Site

Bone Morphogenetic Protein-4 (BMP-4) is a potent epidermal inducer and inhibitor of neural fate. We have used differential screening to identify genes involved in epidermal induction downstream of BMP-4 and report here evidence of a novel translational mechanism that regulates the division of the vertebrate ectoderm into regions of neural and epidermal fate. In dissociated Xenopus ectoderm, addition of ectopic BMP-4 leads to an increase in the expression of translation initiation factor 4AIII (eIF-4AIII), a divergent member of the eIF-4A gene family until now characterized only in plants. In the gastrula embryo, Xenopus eIF-4AIII (XeIF-4AIII) expression is elevated in the ventral ectoderm, a site of active BMP signal transduction. Moreover, overexpression of XeIF-4AIII induces epidermis in dissociated cells that would otherwise adopt a neural fate, mimicking the effects of BMP-4. Epidermal induction by XeIF-4AIII requires both an active BMP signaling pathway and an extracellular intermediate. Our results suggest that XeIF-4AIII can regulate changes in cell fate through selective mRNA translation. We propose that BMPs and XeIF-4AIII interact through a positive feedback loop in the ventral ectoderm of the vertebrate gastrula.

scholarly journals TCam-2 Cells Deficient for SOX2 and FOXA2 Are Blocked in Differentiation and Maintain a Seminoma-Like Cell Fate In Vivo

Cancers ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 728 ◽  
Author(s):  
Daniel Nettersheim ◽  
Saskia Vadder ◽  
Sina Jostes ◽  
Alena Heimsoeth ◽  
Hubert Schorle
Keyword(s):  
Cell Fate ◽  
Primordial Germ Cells ◽  
Germ Cell Tumors ◽  
Embryonic Stem ◽  
Bmp Signaling ◽  
Stem Cell Population ◽  
Testicular Germ Cell ◽  
Key Factor ◽  
Pioneer Factor

Testicular germ cell tumors (GCTs) are very common in young men and can be stratified into seminomas and non-seminomas. While seminomas share a similar gene expression and epigenetic profile with primordial germ cells, the stem cell population of the non-seminomas, the embryonal carcinoma (EC), resembles malignant embryonic stem cells. Thus, ECs are able to differentiate into cells of all three germ layers (teratomas) and even extra-embryonic-tissue-like cells (yolk-sac tumor, choriocarcinoma). In the last years, we demonstrated that the cellular microenvironment considerably influences the plasticity of seminomas (TCam-2 cells). Upon a microenvironment-triggered inhibition of the BMP signaling pathway in vivo (murine flank or brain), seminomatous TCam-2 cells reprogram to an EC-like cell fate. We identified SOX2 as a key factor activated upon BMP inhibition mediating the reprogramming process by regulating pluripotency, reprogramming and epigenetic factors. Indeed, CRISPR/Cas9 SOX2-deleted TCam-2 cells were able to maintain a seminoma-cell fate in vivo for about six weeks, but after six weeks in vivo still small sub-populations initiated differentiation. Closer analyses of these differentiated clusters suggested that the pioneer factor FOXA2 might be the driving force behind this induction of differentiation, since many FOXA2 interacting genes and differentiation factors like AFP, EOMES, CDX1, ALB, HAND1, DKK, DLK1, MSX1 and PITX2 were upregulated. In this study, we generated TCam-2 cells double-deficient for SOX2 and FOXA2 using the CRISPR/Cas9 technique and xenografted those cells into the flank of nude mice. Upon loss of SOX2 and FOXA2, TCam-2 maintained a seminoma cell fate for at least twelve weeks, demonstrating that both factors are key players in the reprogramming to an EC-like cell fate. Therefore, our study adds an important piece to the puzzle of GCT development and plasticity, providing interesting insights in what can be expected in a patient, when GCT cells are confronted with different microenvironments.

scholarly journals Apc deficiency alters pulmonary epithelial cell fate and inhibits Nkx2.1 via triggering TGF-beta signaling

2013 ◽  
Vol 378 (1) ◽  
pp. 13-24 ◽  
Author(s):  
Changgong Li ◽  
Aimin Li ◽  
Yiming Xing ◽  
Min Li ◽  
Belinda Chan ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Fate ◽  
Tgf Beta ◽  
Pulmonary Epithelial Cell

scholarly journals Autophagy Is a Component of Epithelial Cell Fate in Obstructive Uropathy

2010 ◽  
Vol 176 (4) ◽  
pp. 1767-1778 ◽  
Author(s):  
Ling Li ◽  
Diana Zepeda-Orozco ◽  
Rachel Black ◽  
Fangming Lin
Keyword(s):  
Epithelial Cell ◽  
Cell Fate ◽  
Obstructive Uropathy

scholarly journals Medial Edge Epithelial Cell Fate during Palatal Fusion

2000 ◽  
Vol 220 (2) ◽  
pp. 343-357 ◽  
Author(s):  
C. Martı́nez-Álvarez ◽  
C. Tudela ◽  
J. Pérez-Miguelsanz ◽  
S. O'Kane ◽  
J. Puerta ◽  
...  
Keyword(s):  
Epithelial Cell ◽  
Cell Fate ◽  
Palatal Fusion ◽  
Medial Edge
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