器官发育的蓝图已在胚胎发育的早期阶段预设。转录和表观遗传机制被提出来预设发育轨迹。然而，我们揭示了人类胚胎干细胞（hESCs）未来心脏命运的能力是由一种由RBPMS控制的专门的mRNA翻译电路在多能性中预设的。 RBPMS被招募到hESCs中的活性核糖体上，以控制必需的因子的翻译，包括Wingless / Integrated（WNT）信号传导。因此，RBPMS丧失特定和严重妨碍心脏中胚层的规定，导致人类心脏器官的方式和形态缺陷。在机制上，RBPMS通过选择性的3'UTR结合和促进翻译起始的全球特殊化mRNA翻译。因此，RBPMS的丧失导致翻译起始缺陷，其中包括EIF3复合物异常滞留和mRNA中EIF5A的耗竭，从而取消核糖体招募。我们展示了如何通过专门的mRNA翻译在胚胎发育过程中编程未来的命运轨迹。

The blueprints of developing organs are preset at the early stages of embryogenesis. Transcriptional and epigenetic mechanisms are proposed to preset developmental trajectories. However, we reveal that the competence for the future cardiac fate of human embryonic stem cells (hESCs) is preset in pluripotency by a specialized mRNA translation circuit controlled by RBPMS. RBPMS is recruited to active ribosomes in hESCs to control the translation of essential factors needed for cardiac commitment program, including Wingless/Integrated (WNT) signaling. Consequently, RBPMS loss specifically and severely impedes cardiac mesoderm specification, leading to patterning and morphogenetic defects in human cardiac organoids. Mechanistically, RBPMS specializes mRNA translation, selectively via 3'UTR binding and globally by promoting translation initiation. Accordingly, RBPMS loss causes translation initiation defects highlighted by aberrant retention of the EIF3 complex and depletion of EIF5A from mRNAs, thereby abrogating ribosome recruitment. We demonstrate how future fate trajectories are programmed during embryogenesis by specialized mRNA translation.