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Extra-embryonic syndecan 2 regulates organ primordia migration and fibrillogenesis throughout the zebrafish embryo.

机译:胚外syndecan 2调节整个斑马鱼胚胎的器官原基迁移和原纤维形成。

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One of the first steps in zebrafish heart and gut organogenesis is the migration of bilateral primordia to the midline to form cardiac and gut tubes. The mechanisms that regulate this process are poorly understood. Here we show that the proteoglycan syndecan 2 (Sdc2) expressed in the extra-embryonic yolk syncytial layer (YSL) acts locally at the YSL-embryo interface to direct organ primordia migration, and is required for fibronectin and laminin matrix assembly throughout the embryo. Surprisingly, neither endogenous nor exogenous sdc2 expressed in embryonic cells can compensate for knockdown of sdc2 in the YSL, indicating that Sdc2 expressed in extra-embryonic tissues is functionally distinct from Sdc2 in embryonic cells. The effects of sdc2 knockdown in the YSL can be rescued by extra-embryonic Sdc2 lacking an extracellular proteolytic cleavage (shedding) site, but not by extra-embryonic Sdc2 lacking extracellular glycosaminoglycan (GAG) addition sites, suggesting that distinct GAG chains on extra-embryonic Sdc2 regulate extracellular matrix assembly, cell migration and epithelial morphogenesis of multiple organ systems throughout the embryo.
机译:斑马鱼心脏和肠道器官发生的第一步之一是将双侧原基迁移到中线以形成心脏和肠管。调节这一过程的机制了解甚少。在这里我们显示出在胚外卵黄合胞体层(YSL)中表达的蛋白聚糖syndecan 2(Sdc2)在YSL-胚界面处局部起作用,以指导器官原基迁移,并且是纤连蛋白和层粘连蛋白基质组装在整个胚胎中所必需的。出人意料的是,胚胎细胞中表达的内源性和外源性sdc2都无法补偿YSL中sdc2的敲低,这表明胚外组织中表达的Sdc2在功能上不同于胚胎细胞中的Sdc2。可以通过缺少细胞外蛋白水解切割(脱落)位点的胚外Sdc2来挽救YSL中sdc2的影响,但不能通过缺少细胞外糖胺聚糖(GAG)加成位点的胚胎外Sdc2来挽救,这表明在胚胎Sdc2调节整个胚胎中多个器官系统的细胞外基质装配,细胞迁移和上皮形态发生。

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