Sakaguchi Takuya, Kikuchi Yutaka, Kuroiwa Atsushi, Takeda Hiroyuki, Stainier Didier Y R
Department of Biochemistry and Biophysics and Programs in Developmental Biology, Genetics and Human Genetics, Cardiovascular Research Institute, University of California, San Francisco, San Francisco, CA 94143-2711, USA.
Development. 2006 Oct;133(20):4063-72. doi: 10.1242/dev.02581.
The roles of extra-embryonic tissues in early vertebrate body patterning have been extensively studied, yet we know little about their function during later developmental events. Here, we analyze the function of the zebrafish extra-embryonic yolk syncytial layer (YSL) specific transcription factor, Mtx1, and find that it plays an essential role in myocardial migration. Downregulating the function of Mtx1 in the YSL leads to cardia bifida, a phenotype in which the myocardial cells fail to migrate to the midline. Mtx1 in the extra-embryonic YSL appears to regulate the embryonic expression of fibronectin, a gene previously implicated in myocardial migration. We further show dosage-sensitive genetic interactions between mtx1 and fibronectin. Based on these data, we propose that the extra-embryonic YSL regulates myocardial migration, at least in part by influencing fibronectin expression and subsequent assembly of the extracellular matrix in embryonic tissues.
脊椎动物早期胚胎外组织在身体模式形成中的作用已得到广泛研究,但我们对它们在后期发育事件中的功能却知之甚少。在此,我们分析了斑马鱼胚胎外卵黄合胞体层(YSL)特异性转录因子Mtx1的功能,发现它在心肌迁移中起着至关重要的作用。下调YSL中Mtx1的功能会导致心脏分裂,即心肌细胞无法迁移至中线的一种表型。胚胎外YSL中的Mtx1似乎调控纤连蛋白的胚胎表达,纤连蛋白是一个先前被认为与心肌迁移有关的基因。我们进一步展示了mtx1与纤连蛋白之间的剂量敏感型遗传相互作用。基于这些数据,我们提出胚胎外YSL至少部分通过影响纤连蛋白表达以及随后胚胎组织中细胞外基质的组装来调控心肌迁移。