Morasso M I, Grinberg A, Robinson G, Sargent T D, Mahon K A
Laboratory of Molecular Genetics, National Institutes of Health, Bethesda, MD 20892, USA.
Proc Natl Acad Sci U S A. 1999 Jan 5;96(1):162-7. doi: 10.1073/pnas.96.1.162.
Dlx3 is a homeodomain transcription factor and a member of the vertebrate Distal-less family. Targeted deletion of the mouse Dlx3 gene results in embryonic death between day 9.5 and day 10 because of placental defects that alter the development of the labyrinthine layer. In situ hybridization reveals that the Dlx3 gene is initially expressed in ectoplacental cone cells and chorionic plate, and later in the labyrinthine trophoblast of the chorioallantoic placenta, where major defects are observed in the Dlx3 -/- embryos. The expression of structural genes, such as 4311 and PL-1, which were used as markers to follow the fate of different derivatives of the placenta, was not affected in the Dlx3-null embryos. However, by day 10.5 of development, expression of the paired-like homeodomain gene Esx1 was strongly down-regulated in affected placenta tissue, suggesting that Dlx3 is required for the maintenance of Esx1 expression, normal placental morphogenesis, and embryonic survival.
Dlx3是一种同源结构域转录因子，也是脊椎动物远端缺失（Distal-less）家族的成员。靶向敲除小鼠Dlx3基因会导致胚胎在第9.5天至第10天之间死亡，原因是胎盘缺陷改变了迷路层的发育。原位杂交显示，Dlx3基因最初在外胎盘锥体细胞和绒毛膜板中表达，随后在绒毛尿囊胎盘的迷路滋养层中表达，在Dlx3基因敲除的胚胎中，此处观察到主要缺陷。用作追踪胎盘不同衍生物命运标记的结构基因（如4311和PL-1）的表达在Dlx3基因缺失的胚胎中未受影响。然而，在发育到第10.5天时，配对样同源结构域基因Esx1在受影响的胎盘组织中的表达强烈下调，这表明Dlx3是维持Esx1表达、正常胎盘形态发生和胚胎存活所必需的。
