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E-钙黏蛋白在小鼠胚胎干细胞中作为与广泛的细胞过程相关的转录物的调节剂发挥作用。

E-cadherin acts as a regulator of transcripts associated with a wide range of cellular processes in mouse embryonic stem cells.

机构信息

Core Technology Facility, Faculty of Medical and Human Sciences, The University of Manchester, Manchester, United Kingdom.

出版信息

PLoS One. 2011;6(7):e21463. doi: 10.1371/journal.pone.0021463. Epub 2011 Jul 14.

DOI:10.1371/journal.pone.0021463
PMID:21779327
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3136471/
Abstract

BACKGROUND

We have recently shown that expression of the cell adhesion molecule E-cadherin is required for LIF-dependent pluripotency of mouse embryonic stem (ES) cells.

METHODOLOGY

In this study, we have assessed global transcript expression in E-cadherin null (Ecad-/-) ES cells cultured in either the presence or absence of LIF and compared these to the parental cell line wtD3.

RESULTS

We show that LIF has little effect on the transcript profile of Ecad-/- ES cells, with statistically significant transcript alterations observed only for Sp8 and Stat3. Comparison of Ecad-/- and wtD3 ES cells cultured in LIF demonstrated significant alterations in the transcript profile, with effects not only confined to cell adhesion and motility but also affecting, for example, primary metabolic processes, catabolism and genes associated with apoptosis. Ecad-/- ES cells share similar, although not identical, gene expression profiles to epiblast-derived pluripotent stem cells, suggesting that E-cadherin expression may inhibit inner cell mass to epiblast transition. We further show that Ecad-/- ES cells maintain a functional β-catenin pool that is able to induce β-catenin/TCF-mediated transactivation but, contrary to previous findings, do not display endogenous β-catenin/TCF-mediated transactivation. We conclude that loss of E-cadherin in mouse ES cells leads to significant transcript alterations independently of β-catenin/TCF transactivation.

摘要

背景

我们最近发现，细胞黏附分子 E-钙黏蛋白的表达对于 LIF 依赖性的小鼠胚胎干细胞（ES 细胞）多能性是必需的。

方法

在本研究中，我们评估了在存在或不存在 LIF 的情况下培养的 E-钙黏蛋白缺失（Ecad-/-）ES 细胞中的全局转录表达，并将其与亲本细胞系 wtD3 进行了比较。

结果

我们表明，LIF 对 Ecad-/-ES 细胞的转录谱几乎没有影响，仅观察到 Sp8 和 Stat3 的转录发生了统计学上显著的改变。在 LIF 中培养的 Ecad-/-和 wtD3 ES 细胞之间的比较显示，转录谱发生了显著改变，这些影响不仅局限于细胞黏附和运动，还影响了例如初级代谢过程、分解代谢以及与凋亡相关的基因。Ecad-/-ES 细胞与内细胞团衍生的多能性干细胞具有相似的基因表达谱，尽管不完全相同，这表明 E-钙黏蛋白的表达可能抑制了内细胞团向上胚层的转变。我们进一步表明，Ecad-/-ES 细胞保持了功能性的β-连环蛋白池，能够诱导β-连环蛋白/TCF 介导的转录激活，但与先前的发现相反，它们不显示内源性β-连环蛋白/TCF 介导的转录激活。我们得出结论，在小鼠 ES 细胞中缺失 E-钙黏蛋白会导致显著的转录改变，而不依赖于β-连环蛋白/TCF 转录激活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc7/3136471/59f0caa0561d/pone.0021463.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc7/3136471/8d2051ed2865/pone.0021463.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc7/3136471/90f019835c96/pone.0021463.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc7/3136471/6dc7315210f2/pone.0021463.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc7/3136471/1b4e1add6198/pone.0021463.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc7/3136471/fed7d5e0c206/pone.0021463.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc7/3136471/59f0caa0561d/pone.0021463.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc7/3136471/8d2051ed2865/pone.0021463.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc7/3136471/90f019835c96/pone.0021463.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc7/3136471/6dc7315210f2/pone.0021463.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc7/3136471/1b4e1add6198/pone.0021463.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc7/3136471/fed7d5e0c206/pone.0021463.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6fc7/3136471/59f0caa0561d/pone.0021463.g006.jpg

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