In:
eLife, eLife Sciences Publications, Ltd, Vol. 6 ( 2017-12-19)
Kurzfassung:
Deletion of Sox2 from mouse embryonic stem cells (ESCs) causes trophectodermal differentiation. While this can be prevented by enforced expression of the related SOXB1 proteins, SOX1 or SOX3, the roles of SOXB1 proteins in epiblast stem cell (EpiSC) pluripotency are unknown. Here, we show that Sox2 can be deleted from EpiSCs with impunity. This is due to a shift in the balance of SoxB1 expression in EpiSCs, which have decreased Sox2 and increased Sox3 compared to ESCs. Consistent with functional redundancy, Sox3 can also be deleted from EpiSCs without eliminating self-renewal. However, deletion of both Sox2 and Sox3 prevents self-renewal. The overall SOXB1 levels in ESCs affect differentiation choices: neural differentiation of Sox2 heterozygous ESCs is compromised, while increased SOXB1 levels divert the ESC to EpiSC transition towards neural differentiation. Therefore, optimal SOXB1 levels are critical for each pluripotent state and for cell fate decisions during exit from naïve pluripotency.
Materialart:
Online-Ressource
ISSN:
2050-084X
DOI:
10.7554/eLife.27746.001
DOI:
10.7554/eLife.27746.002
DOI:
10.7554/eLife.27746.003
DOI:
10.7554/eLife.27746.004
DOI:
10.7554/eLife.27746.005
DOI:
10.7554/eLife.27746.006
DOI:
10.7554/eLife.27746.007
DOI:
10.7554/eLife.27746.008
DOI:
10.7554/eLife.27746.009
DOI:
10.7554/eLife.27746.010
DOI:
10.7554/eLife.27746.011
DOI:
10.7554/eLife.27746.012
DOI:
10.7554/eLife.27746.013
DOI:
10.7554/eLife.27746.014
DOI:
10.7554/eLife.27746.015
DOI:
10.7554/eLife.27746.016
DOI:
10.7554/eLife.27746.017
DOI:
10.7554/eLife.27746.018
DOI:
10.7554/eLife.27746.019
DOI:
10.7554/eLife.27746.020
DOI:
10.7554/eLife.27746.021
DOI:
10.7554/eLife.27746.022
DOI:
10.7554/eLife.27746.023
DOI:
10.7554/eLife.27746.024
DOI:
10.7554/eLife.27746.025
DOI:
10.7554/eLife.27746.026
DOI:
10.7554/eLife.27746.027
DOI:
10.7554/eLife.27746.028
DOI:
10.7554/eLife.27746.029
DOI:
10.7554/eLife.27746.033
DOI:
10.7554/eLife.27746.034
Sprache:
Englisch
Verlag:
eLife Sciences Publications, Ltd
Publikationsdatum:
2017
ZDB Id:
2687154-3
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