Gene regulatory networks and developmental plasticity in the early sea urchin embryo: alternative deployment of the skeletogenic gene regulatory network
Gene regulatory networks and developmental plasticity in the early sea urchin embryo: alternative deployment of the skeletogenic gene regulatory network
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DOI：
10.1242/dev.009092
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发表时间：
2007-09-01
期刊：
影响因子：
4.6
通讯作者：
Sharma, Tara
中科院分区：
文献类型：
--
作者：
Ettensohn, Charles A.;Kitazawa, Chisato;Sharma, Tara
海胆胚胎中的细胞命运是非常不稳定的，尽管事实上，母体极性和合子程序的差异基因表达模式的胚胎从最早的阶段。最近的工作集中在转录基因调控网络（GRNs）部署在特定的胚胎领土在早期发展。微团-初级间充质细胞（PMC）GRN驱动胚胎骨骼的发育。虽然通常只由假定的PMC部署，但早期胚胎的每个谱系都有激活这一途径的潜力。在这里，我们专注于一个引人注目的例子，调节激活的骨骼GRN的非骨骼中胚层（NSM）细胞的PMC的命运在原肠胚形成的。我们发现，伴随着重新表达的终端，生物矿化相关基因的PMC GRN，以及编码两个上游转录因子，Lvalx 1和Lvtbr的基因。我们报告说，Lvalx 1，PMC谱系中的成骨GRN的关键组成部分，在NSM细胞和动物卵裂球的调节途径中起着至关重要的作用。NSM细胞中Lvalx 1和下游骨骼发生基因的表达需要MAPK信号传导，反映了其在PMC谱系中的作用。我们还表明，Lvalx 1调节的信号，通常抑制NSM的pmc。值得注意的是，Lvalx 1在大单体（NSM细胞的祖细胞）中的错误表达足以激活骨骼生成GRN。我们认为，NSM细胞通常部署的基础中胚层途径，只需要一个Lvalx 1介导的子程序来表达PMC的命运。最后，我们提供的证据表明，在正常的途径，激活的骨骼GRN在NSM细胞是独立的Lvpmar 1。我们的研究表明，虽然大多数功能的micromere-PMC的GRN的重演在nSM细胞，不同的输入激活这个GRN在正常和调节发展。
Cell fates in the sea urchin embryo are remarkably labile, despite the fact that maternal polarity and zygotic programs of differential gene expression pattern the embryo from the earliest stages. Recent work has focused on transcriptional gene regulatory networks (GRNs) deployed in specific embryonic territories during early development. The micromere-primary mesenchyme cell (PMC) GRN drives the development of the embryonic skeleton. Although normally deployed only by presumptive PMCs, every lineage of the early embryo has the potential to activate this pathway. Here, we focus on one striking example of regulative activation of the skeletogenic GRN; the transfating of non-skeletogenic mesoderm (NSM) cells to a PMC fate during gastrulation. We show that transfating is accompanied by the de novo expression of terminal, biomineralization-related genes in the PMC GRN, as well as genes encoding two upstream transcription factors, Lvalx1 and Lvtbr. We report that Lvalx1, a key component of the skeletogenic GRN in the PMC lineage, plays an essential role in the regulative pathway both in NSM cells and in animal blastomeres. MAPK signaling is required for the expression of Lvalx1 and downstream skeletogenic genes in NSM cells, mirroring its role in the PMC lineage. We also demonstrate that Lvalx1 regulates the signal from PMCs that normally suppresses NSM transfating. Significantly, misexpression of Lvalx1 in macromeres (the progenitors of NSM cells) is sufficient to activate the skeletogenic GRN. We suggest that NSM cells normally deploy a basal mesodermal pathway and require only an Lvalx1-mediated sub-program to express a PMC fate. Finally, we provide evidence that, in contrast to the normal pathway, activation of the skeletogenic GRN in NSM cells is independent of Lvpmar1. Our studies reveal that, although most features of the micromere-PMC GRN are recapitulated in transfating NSM cells, different inputs activate this GRN during normal and regulative development.