Department of Cell Biology, Neurobiology and Anatomy, Medical College of Wisconsin, Milwaukee, United States.
Division of Biostatistics, Institute for Health and Equity, Medical College of Wisconsin, Milwaukee, United States.
Elife. 2024 Jul 25;12:RP89367. doi: 10.7554/eLife.89367.
Amniogenesis, a process critical for continuation of healthy pregnancy, is triggered in a collection of pluripotent epiblast cells as the human embryo implants. Previous studies have established that bone morphogenetic protein (BMP) signaling is a major driver of this lineage specifying process, but the downstream BMP-dependent transcriptional networks that lead to successful amniogenesis remain to be identified. This is, in part, due to the current lack of a robust and reproducible model system that enables mechanistic investigations exclusively into amniogenesis. Here, we developed an improved model of early amnion specification, using a human pluripotent stem cell-based platform in which the activation of BMP signaling is controlled and synchronous. Uniform amniogenesis is seen within 48 hr after BMP activation, and the resulting cells share transcriptomic characteristics with amnion cells of a gastrulating human embryo. Using detailed time-course transcriptomic analyses, we established a previously uncharacterized BMP-dependent amniotic transcriptional cascade, and identified markers that represent five distinct stages of amnion fate specification; the expression of selected markers was validated in early post-implantation macaque embryos. Moreover, a cohort of factors that could potentially control specific stages of amniogenesis was identified, including the transcription factor TFAP2A. Functionally, we determined that, once amniogenesis is triggered by the BMP pathway, TFAP2A controls the progression of amniogenesis. This work presents a temporally resolved transcriptomic resource for several previously uncharacterized amniogenesis states and demonstrates a critical intermediate role for TFAP2A during amnion fate specification.
羊膜发生,是人类胚胎着床时多能胚外细胞系中触发的一个关键过程,对于维持健康妊娠至关重要。先前的研究已经确定,骨形态发生蛋白(BMP)信号是这个谱系特化过程的主要驱动因素,但导致成功羊膜发生的下游 BMP 依赖性转录网络仍有待确定。部分原因是目前缺乏一个强大且可重复的模型系统,该系统可以专门用于羊膜发生的机制研究。在这里,我们使用基于人类多能干细胞的平台开发了一种早期羊膜特化的改良模型,其中 BMP 信号的激活是可控且同步的。在 BMP 激活后 48 小时内即可观察到均匀的羊膜发生,并且得到的细胞与正在进行原肠胚形成的人类胚胎的羊膜细胞具有转录组特征。通过详细的时间过程转录组分析,我们建立了一个以前未被描述的 BMP 依赖性羊膜转录级联,并确定了代表羊膜命运特化的五个不同阶段的标记物;选择的标记物的表达在早期植入后猕猴胚胎中得到了验证。此外,还确定了一组可能控制羊膜发生特定阶段的因子,包括转录因子 TFAP2A。功能上,我们确定一旦 BMP 途径触发了羊膜发生,TFAP2A 就会控制羊膜发生的进程。这项工作为几个以前未被描述的羊膜发生状态提供了一个时间分辨的转录组资源,并证明了 TFAP2A 在羊膜命运特化过程中起着关键的中间作用。