Birth Defects Center, University of Louisville, 501 South Preston Street, Suite 350, Louisville, KY 40202, USA.
Cell Tissue Res. 2013 Mar;351(3):445-52. doi: 10.1007/s00441-012-1525-2. Epub 2012 Nov 13.
Loss of Prdm16 expression in the mouse leads to a complete cleft of the secondary palate. We have now determined changes in gene expression in the secondary palates of Prdm16(-/-) fetuses in an attempt to reveal the mechanism(s) leading to the failure of palate closure in these mice. Defined pathway-based polymerase chain reaction arrays were used to analyze the expression of genes associated with the extracellular matrix and the transforming growth factor-β and bone morphogenetic protein signaling networks, perturbations of which can lead to palatal clefting. Loss of Prdm16 expression in the secondary palate leads to alterations in numerous genes within these groups, many of which have been linked to chondrogenesis and osteogenesis. The expression of several genes linked to bone development was significantly changed in the developing secondary palate. Analysis of gene expression in the mandibles of Prdm16(-/-) fetuses revealed similar alterations in the same gene set. These data suggest that one function of Prdm16 is the regulation of genes that play a role in the differentiation of mesenchymal cells into chondro-/osteocytes.
Prdm16 表达缺失导致小鼠的次级腭完全裂开。我们现在已经确定了 Prdm16(-/-)胎鼠次级腭中基因表达的变化,试图揭示导致这些小鼠腭闭合失败的机制。使用定义的基于途径的聚合酶链反应阵列分析与细胞外基质和转化生长因子-β和骨形态发生蛋白信号网络相关的基因表达,这些网络的干扰可导致腭裂。次级腭中 Prdm16 表达的缺失导致这些组内许多基因的改变,其中许多基因与软骨生成和骨生成有关。与骨发育相关的几个基因的表达在发育中的次级腭中发生了显著改变。对 Prdm16(-/-)胎鼠下颌骨的基因表达分析显示,相同基因集中也存在类似的改变。这些数据表明,Prdm16 的一个功能是调节在间充质细胞分化为软骨/成骨细胞中起作用的基因。