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苏氨酸磷酸化对于 OCT4 与 SOX2 维持小鼠胚胎干细胞多能性的相互作用至关重要。

Phosphorylation of Threonine Is Crucial for OCT4 Interaction with SOX2 in the Maintenance of Mouse Embryonic Stem Cell Pluripotency.

机构信息

Department of Cell Biology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China.

Shanghai Advanced Research Institute, Chinese Academy of Sciences, Shanghai 201210, China; School of Life Science and Technology, ShanghaiTech University, Shanghai 201210, China; University of Chinese Academy of Sciences, Beijing 100049, China; Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.

出版信息

Stem Cell Reports. 2017 Nov 14;9(5):1630-1641. doi: 10.1016/j.stemcr.2017.09.001. Epub 2017 Oct 5.

DOI:10.1016/j.stemcr.2017.09.001
PMID:28988986
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5829306/
Abstract

OCT4 is required to maintain the pluripotency of embryonic stem cells (ESCs); yet, overdose-expression of OCT4 induces ESC differentiation toward primitive endoderm. The molecular mechanism underlying this differentiation switch is not fully understood. Here, we found that substitution of threonine by alanine (T343A), but not aspartic acid (T343D), caused a significant loss of OCT4-phosphorylation signal in ESCs. Loss of such OCT4-phosphorylation compromises its interaction with SOX2 but promotes interaction with SOX17. We therefore propose that threonine-based OCT4-phosphorylation is crucial for the maintenance of ESC pluripotency. This OCT4-phosphorylation-based mechanism may provide insight into the regulation of lineage specification during early embryonic development.

摘要

OCT4 对于维持胚胎干细胞（ESCs）的多能性至关重要；然而，OCT4 的过表达会诱导 ESC 向原始内胚层分化。这种分化开关的分子机制尚不完全清楚。在这里，我们发现苏氨酸被丙氨酸（T343A）取代，而不是天冬氨酸（T343D），会导致 ESCs 中 OCT4 磷酸化信号的显著丢失。这种 OCT4 磷酸化的丢失会损害其与 SOX2 的相互作用，但会促进与 SOX17 的相互作用。因此，我们提出基于苏氨酸的 OCT4 磷酸化对于维持 ESC 的多能性至关重要。这种基于 OCT4 磷酸化的机制可能为早期胚胎发育过程中谱系特化的调控提供了新的见解。

相似文献

[1]
Phosphorylation of Threonine Is Crucial for OCT4 Interaction with SOX2 in the Maintenance of Mouse Embryonic Stem Cell Pluripotency.

Stem Cell Reports. 2017-10-5

[2]
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J Biol Chem. 2018-1-29

[3]
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[4]
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[5]
Simultaneous targeted inhibition of Sox2-Oct4 transcription factors using decoy oligodeoxynucleotides to repress stemness properties in mouse embryonic stem cells.

Cell Biol Int. 2017-12

[6]
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Sci Rep. 2015-8-28

[7]
Tgif1 Counterbalances the Activity of Core Pluripotency Factors in Mouse Embryonic Stem Cells.

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[8]
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[9]
Interplay of Oct4 with Sox2 and Sox17: a molecular switch from stem cell pluripotency to specifying a cardiac fate.

J Cell Biol. 2009-9-7

[10]
Transient pairing of homologous Oct4 alleles accompanies the onset of embryonic stem cell differentiation.

Cell Stem Cell. 2015-3-5

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[5]
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[6]
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[7]
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[8]
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[9]
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[10]
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本文引用的文献

[1]
Parkinson-associated risk variant in distal enhancer of α-synuclein modulates target gene expression.

Nature. 2016-5-5

[2]
Lineage specification in the mouse preimplantation embryo.

Development. 2016-4-1

[3]
Akt‑mediated phosphorylation of Oct4 is associated with the proliferation of stem‑like cancer cells.

Oncol Rep. 2015-4

[4]
Rbm46 regulates trophectoderm differentiation by stabilizing Cdx2 mRNA in early mouse embryos.

Stem Cells Dev. 2015-4-1

[5]
Induction of pluripotency in mouse somatic cells with lineage specifiers.

Cell. 2013-5-23

[6]
Oct4 switches partnering from Sox2 to Sox17 to reinterpret the enhancer code and specify endoderm.

EMBO J. 2013-3-8

[7]
Reciprocal regulation of Akt and Oct4 promotes the self-renewal and survival of embryonal carcinoma cells.

Mol Cell. 2012-10-4

[8]
Serine 111 phosphorylation regulates OCT4A protein subcellular distribution and degradation.

J Biol Chem. 2012-9-28

[9]
Phosphorylation regulates human OCT4.

Proc Natl Acad Sci U S A. 2012-4-2

[10]
Primitive endoderm differentiates via a three-step mechanism involving Nanog and RTK signaling.

Dev Cell. 2011-12-13

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