The mammalian decidual cell evolved from a cellular stress response.
The mammalian decidual cell evolved from a cellular stress response.
复制标题
DOI：
10.1371/journal.pbio.2005594
复制
发表时间：
2018-08
期刊：
影响因子：
9.8
通讯作者：
Wagner GP
中科院分区：
文献类型：
--
作者：
Erkenbrack EM;Maziarz JD;Griffith OW;Liang C;Chavan AR;Nnamani MC;Wagner GP
在动物物种中，细胞类型在数量和种类上差异很大。生物体中发现的细胞类型数量在物种之间存在很大差异，细胞类型多样性是生物体结构和功能差异的重要贡献者。这些观察结果表明细胞类型起源是进化新颖性的重要来源。然而，人们对导致新型细胞类型进化的分子机制知之甚少。在这里，我们展示了真兽类哺乳动物的一种新型细胞类型，即蜕膜基质细胞（DSC），是通过重新连接祖先细胞应激反应而进化而来的。我们从负鼠 Monodelphis Domestica 中分离出 DSC 的前体细胞类型，即子宫内膜基质成纤维细胞 (ESF)。我们发现，在负鼠 ESF 中，大多数蜕膜核心调节基因对蜕膜化信号做出反应，但不调节蜕膜效应基因。相反，在负鼠 ESF 中，蜕膜转录因子在细胞凋亡和氧化应激反应中发挥作用。我们认为细胞应激反应的重新连接是真兽类蜕膜细胞类型进化的重要机制。动物由多种细胞组成，根据它们在体内的位置发挥不同的功能。不同动物物种中具有相似功能或细胞类型的细胞通过进化血统（类似于物种本身的相关性）和胚胎发育血统相关。相互作用的基因网络或基因调控网络控制细胞中的基因表达，从而指定细胞类型的身份。了解新细胞类型如何通过改变基因调控网络产生对于理解人类生物学的基本方面和在实验室中操纵细胞类型至关重要。我们通过研究来自人类和负鼠（两种远亲哺乳动物）子宫的子宫内膜基质成纤维细胞（ESF）来解决这个问题。我们发现负鼠的远亲细胞类型表达了一组与人类细胞相似的调节基因，但为了响应与妊娠相关的信号，负鼠细胞会诱导应激反应。在人类细胞中，这些信号诱导分化为蜕膜细胞，这是人类和密切相关的哺乳动物中存在的一种特殊细胞类型。这些结果表明，调节祖先的、与妊娠相关的应激反应的基因调控网络被劫持并重新用于在蜕膜细胞类型的分化和规范中发挥作用。
Among animal species, cell types vary greatly in terms of number and kind. The number of cell types found within an organism differs considerably between species, and cell type diversity is a significant contributor to differences in organismal structure and function. These observations suggest that cell type origination is a significant source of evolutionary novelty. The molecular mechanisms that result in the evolution of novel cell types, however, are poorly understood. Here, we show that a novel cell type of eutherians mammals, the decidual stromal cell (DSC), evolved by rewiring an ancestral cellular stress response. We isolated the precursor cell type of DSCs, endometrial stromal fibroblasts (ESFs), from the opossum Monodelphis domestica. We show that, in opossum ESFs, the majority of decidual core regulatory genes respond to decidualizing signals but do not regulate decidual effector genes. Rather, in opossum ESFs, decidual transcription factors function in apoptotic and oxidative stress response. We propose that rewiring of cellular stress responses was an important mechanism for the evolution of the eutherian decidual cell type. Animals consist of a wide variety of cells that serve different functions depending on their location in the body. Cells with similar functions, or cell types, in different animal species are related both by an evolutionary line of descent—similar to the relatedness of species themselves—and by a developmental line of descent in the embryo. Networks of interacting genes, or gene regulatory networks, control gene expression in the cell, thereby specifying cell type identity. Understanding how new cell types arise by changing gene regulatory networks is critical both to comprehending fundamental aspects of human biology and to manipulating cell types in the laboratory. We approached this question by studying endometrial stromal fibroblast (ESF) cells from the uterus of humans and opossums, two distantly related mammals. We showed that the distantly related cell type in opossum expresses a similar set of regulatory genes as the human cell, but in response to pregnancy-related signals, the opossum cells induce a stress response. In the human cells, these signals induce differentiation into decidual cells, a specialized cell type present in humans and closely related mammals. These results suggest that a gene regulatory network that modulated an ancestral, pregnancy-related stress response was hijacked and repurposed to function in differentiation and specification of the decidual cell type.
登录
查看更多内容
DOI：
10.1093/bioinformatics/btu638
发表时间：
2015-01-15
期刊：
Bioinformatics (Oxford, England)
影响因子：
--
作者：
Anders S;Pyl PT;Huber W
通讯作者：
Huber W
影响因子：
4
作者：
Huang, Haojie;Tindall, Donald J.
通讯作者：
Tindall, Donald J.
影响因子：
3.6
作者：
Gendron, RL;Paradis, H;Markoff, E
通讯作者：
Markoff, E
Runx1在小鼠围着床期子宫中的差异表达及调控
影响因子：
3.6
作者：
Bai, Zhi-Kun;Li, Dang-Dang;Yue, Zhan-Peng
通讯作者：
Yue, Zhan-Peng
影响因子：
4.8
作者：
Al-Sabbagh, Marwa;Fusi, Luca;Brosens, Jan J.
通讯作者：
Brosens, Jan J.