Abstract：
Cajal-Retzius cells (CRs) are key players in cerebral cortex development, and they display a unique transcriptomic identity. Here, we use scRNA-seq to reconstruct the differentiation trajectory of mouse hem-derived CRs, and we unravel the transient expression of a complete gene module previously known to control multiciliogenesis. However, CRs do not undergo centriole amplification or multiciliation. Upon deletion of Gmnc, the master regulator of multiciliogenesis, CRs are initially produced but fail to reach their normal identity resulting in their massive apoptosis. We further dissect the contribution of multiciliation effector genes and identify Trp73 as a key determinant. Finally, we use in utero electroporation to demonstrate that the intrinsic competence of hem progenitors as well as the heterochronic expression of Gmnc prevent centriole amplification in the CR lineage. Our work exemplifies how the co-option of a complete gene module, repurposed to control a distinct process, may contribute to the emergence of novel cell identities.
摘要：
Cajal-Retzius细胞（CRs）是大脑皮层发育的关键参与者，它们显示出独特的转录组身份。这里,我们使用scRNA-seq重建小鼠hem来源的CRs的分化轨迹，我们解开了一个完整的基因模块的瞬时表达，这个模块是以前已知的控制多毛发生的。然而,CRs不经历中心粒扩增或多重化。删除GMNC后，多毛生成的主要调节因子，CR最初是产生的，但未能达到其正常身份，导致其大量凋亡。我们进一步剖析了多群体效应基因的贡献，并将Trp73确定为关键决定因素。最后,我们使用子宫内电穿孔来证明hem祖细胞的内在能力以及Gmnc的异慢性表达阻止了CR谱系中的centriole扩增。我们的工作证明了一个完整的基因模块的共同选择，重新用于控制一个独特的过程，可能有助于新细胞身份的出现。
