scholarly journals The transcription factor E2A drives neural differentiation in pluripotent cells

Development ◽  
2020 ◽  
Vol 147 (12) ◽  
pp. dev184093
Author(s):  
Chandrika Rao ◽  
Mattias Malaguti ◽  
John O. Mason ◽  
Sally Lowell
Keyword(s):  
Transcription Factor ◽  
Neural Differentiation ◽  
Pluripotent Cells

scholarly journals The transcription factor E2A drives neural differentiation in pluripotent cells

2019 ◽  
Author(s):  
Chandrika Rao ◽  
Mattias Malaguti ◽  
John O. Mason ◽  
Sally Lowell
Keyword(s):  
Transcription Factor ◽  
Neural Differentiation ◽  
Bhlh Transcription Factor ◽  
Pluripotent Cells ◽  
Neural Lineage ◽  
Binding Partner ◽  
Helix Loop Helix ◽  
Id Proteins ◽  
Mouse Cells ◽  
Extracellular Signalling

AbstractThe intrinsic mechanisms that link extracellular signalling to the onset of neural differentiation are not well understood. In pluripotent mouse cells, BMP blocks entry into the neural lineage via transcriptional upregulation of Inhibitor of Differentiation (Id) factors. We have previously identified that the major binding partner of Id proteins in pluripotent cells is the basic helix-loop-helix (bHLH) transcription factor (TF), E2A. Id1 can prevent E2A from forming heterodimers with bHLH TFs or from forming homodimers. Here, we show that overexpression of a forced E2A homodimer is sufficient to drive robust neural commitment in pluripotent cells, even under non-permissive conditions. Conversely, we find that E2A null cells display a defect in their neural differentiation capacity. E2A acts as an upstream activator of neural lineage genes, including Sox1 and Foxd4, and as a repressor of Nodal signalling. Our results suggest a crucial role for E2A in establishing neural lineage commitment in pluripotent cells.

scholarly journals The BTB transcription factors ZBTB11 and ZFP131 maintain pluripotency by pausing POL II at pro-differentiation genes

2020 ◽  
Author(s):  
Görkem Garipler ◽  
Congyi Lu ◽  
Alexis Morrissey ◽  
Lorena S. Lopez-Zepeda ◽  
Simon E. Vidal ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Stem Cell ◽  
Transcription Factors ◽  
Embryonic Stem ◽  
Loss Of Function ◽  
Pluripotent Cells ◽  
Pol Ii ◽  
Crispr Screen ◽  
Rapid Activation ◽  
Factor Release

AbstractIn pluripotent cells, a delicate activation-repression balance maintains pro-differentiation genes ready for rapid activation. The identity of transcription factors (TFs) that specifically repress pro-differentiation genes remains obscure. By targeting ~1,700 TFs with CRISPR loss-of-function screen, we found that ZBTB11 and ZFP131 are required for embryonic stem cell (ESC) pluripotency. ZBTB11 and ZFP131 maintain promoter-proximally paused Polymerase II at pro-differentiation genes in ESCs. ZBTB11 or ZFP131 loss leads to NELF pausing factor release, an increase in H3K4me3, and transcriptional upregulation of genes associated with all three germ layers. Together, our results suggest that ZBTB11 and ZFP131 maintain pluripotency by preventing premature expression of pro-differentiation genes and present a generalizable framework to maintain cellular potency.One-sentence summaryA Transcription Factor-wide CRISPR screen identifies ZBTB11 and ZFP131 maintaining pluripotency by pausing POL II at pro-differentiation genes

scholarly journals miR-203 imposes an intrinsic barrier during cellular reprogramming by targeting NFATC2

2020 ◽  
Author(s):  
María Salazar-Roa ◽  
Sara Martínez-Martínez ◽  
Osvaldo Graña-Castro ◽  
Mónica Álvarez-Fernández ◽  
Marianna Trakala ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Cellular Reprogramming ◽  
Pluripotent Cells ◽  
Multiple Functions ◽  
Genetic Ablation ◽  
Cellular Models ◽  
Reprogramming Factors ◽  
Early Phases

AbstractCellular reprogramming from somatic to pluripotent cells is the basis for multiple applications aimed to replace damaged tissues in regenerative medicine. However, this process is limited by intrinsic barriers that are induced in response to reprogramming factors. In this manuscript we report that miR-203, a microRNA with multiple functions in differentiation and tumor suppression, acts as an endogenous barrier to reprogramming. Genetic ablation of miR-203 results in enhanced reprogramming whereas its expression prevents the formation of pluripotent cells both in vitro and in vivo. Mechanistically, this effect correlates with the direct repression of NFATC2, a transcription factor involved in the early phases of reprogramming. Inhibition of NFATC2 mimics miR-203 effects whereas NFATC2 overexpression rescues inducible cell pluripotency in miR-203-overexpressing cultures. These data suggest that miR-203 repression may favor the efficiency of reprogramming in a variety of cellular models.

Neural differentiation of pluripotent cells in 3D alginate-based cultures

Biomaterials ◽  
2014 ◽  
Vol 35 (16) ◽  
pp. 4636-4645 ◽  
Author(s):  
Angela Bozza ◽  
Emily E. Coates ◽  
Tania Incitti ◽  
Kimberly M. Ferlin ◽  
Andrea Messina ◽  
...  
Keyword(s):  
Neural Differentiation ◽  
Pluripotent Cells

Forkhead family transcription factor FoxO and neural differentiation

Neurogenetics ◽  
2012 ◽  
Vol 13 (2) ◽  
pp. 105-113 ◽  
Author(s):  
Qiang Wen ◽  
Haitao Wang ◽  
Peter J. Little ◽  
Remi Quirion ◽  
Wenhua Zheng
Keyword(s):  
Transcription Factor ◽  
Neural Differentiation

scholarly journals CTCF is a barrier for 2C-like reprogramming

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Teresa Olbrich ◽  
Maria Vega-Sendino ◽  
Desiree Tillo ◽  
Wei Wu ◽  
Nicholas Zolnerowich ◽  
...  
Keyword(s):  
Dna Damage ◽  
Transcription Factor ◽  
Transcriptional Activation ◽  
Binding Sites ◽  
Neural Progenitor Cells ◽  
Ctcf Binding ◽  
Pluripotent Cells ◽  
Embryonic Tissues ◽  
Binding Factor ◽  
Molecular Determinants

AbstractTotipotent cells have the ability to generate embryonic and extra-embryonic tissues. Interestingly, a rare population of cells with totipotent-like potential, known as 2 cell (2C)-like cells, has been identified within ESC cultures. They arise from ESC and display similar features to those found in the 2C embryo. However, the molecular determinants of 2C-like conversion have not been completely elucidated. Here, we show that the CCCTC-binding factor (CTCF) is a barrier for 2C-like reprogramming. Indeed, forced conversion to a 2C-like state by the transcription factor DUX is associated with DNA damage at a subset of CTCF binding sites. Depletion of CTCF in ESC efficiently promotes spontaneous and asynchronous conversion to a 2C-like state and is reversible upon restoration of CTCF levels. This phenotypic reprogramming is specific to pluripotent cells as neural progenitor cells do not show 2C-like conversion upon CTCF-depletion. Furthermore, we show that transcriptional activation of the ZSCAN4 cluster is necessary for successful 2C-like reprogramming. In summary, we reveal an unexpected relationship between CTCF and 2C-like reprogramming.

Induction of neural differentiation by the transcription factor NeuroD2

2011 ◽  
Vol 30 (2) ◽  
pp. 105-112 ◽  
Author(s):  
Kirsten Messmer ◽  
Wei‐Bin Shen ◽  
Mary Remington ◽  
Paul S. Fishman
Keyword(s):  
Transcription Factor ◽  
Neural Differentiation

scholarly journals Repressor Element 1 Silencing Transcription Factor Couples Loss of Pluripotency with Neural Induction and Neural Differentiation

Stem Cells ◽  
2012 ◽  
Vol 30 (3) ◽  
pp. 425-434 ◽  
Author(s):  
Chiara Soldati ◽  
Angela Bithell ◽  
Caroline Johnston ◽  
Kee-Yew Wong ◽  
Siaw-Wei Teng ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Neural Differentiation ◽  
Neural Induction ◽  
Repressor Element

scholarly journals miR-124, -128, and -137 Orchestrate Neural Differentiation by Acting on Overlapping Gene Sets Containing a Highly Connected Transcription Factor Network

Stem Cells ◽  
2015 ◽  
Vol 34 (1) ◽  
pp. 220-232 ◽  
Author(s):  
Márcia C. T. Santos ◽  
Allison N. Tegge ◽  
Bruna R. Correa ◽  
Swetha Mahesula ◽  
Luana Q. Kohnke ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Neural Differentiation ◽  
Transcription Factor Network ◽  
Overlapping Gene ◽  
Gene Sets
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