Murko Christina, Bronner Marianne E
Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, United States.
Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, United States.
Dev Biol. 2017 Feb 1;422(1):47-57. doi: 10.1016/j.ydbio.2016.12.004. Epub 2016 Dec 22.
The transcription factor Sox10 is a key regulator of vertebrate neural crest development and serves crucial functions in the differentiation of multiple neural crest lineages. In the chick neural crest, two cis-regulatory elements have been identified that mediate Sox10 expression: Sox10E2, which initiates expression in cranial neural crest; Sox10E1 driving expression in vagal and trunk neural crest. Both also mediate Sox10 expression in the otic placode. Here, we have dissected and analyzed the Sox10E1 enhancer element to identify upstream regulatory inputs. Via mutational analysis, we found two critical Sox sites with differential impact on trunk versus otic Sox10E1 mediated reporter expression. Mutation of a combined SoxD/E motif was sufficient to completely abolish neural crest but not ear enhancer activity. However, mutation of both the SoxD/E and another SoxE site eliminated otic Sox10E1 expression. Loss-of-function experiments reveal Sox5 and Sox8 as critical inputs for trunk neural crest enhancer activity, but only Sox8 for its activity in the ear. Finally, we show by ChIP and co-immunoprecipitation that Sox5 directly binds to the SoxD/E site, and that it can interact with Sox8, further supporting their combinatorial role in activation of Sox10E1 in the trunk neural crest. The results reveal important tissue-specific inputs into Sox10 expression in the developing embryo.
转录因子Sox10是脊椎动物神经嵴发育的关键调节因子,在多个神经嵴谱系的分化中发挥着至关重要的作用。在鸡的神经嵴中,已鉴定出两个介导Sox10表达的顺式调节元件:Sox10E2,其在颅神经嵴中启动表达;Sox10E1驱动迷走神经和躯干神经嵴中的表达。两者还介导耳基板中Sox10的表达。在这里,我们剖析并分析了Sox10E1增强子元件,以确定上游调节输入。通过突变分析,我们发现了两个对躯干与耳Sox10E1介导的报告基因表达有不同影响的关键Sox位点。SoxD/E基序组合的突变足以完全消除神经嵴,但不会消除耳增强子活性。然而,SoxD/E和另一个SoxE位点的突变都消除了耳Sox10E1的表达。功能丧失实验表明,Sox5和Sox8是躯干神经嵴增强子活性的关键输入,但只有Sox8对其在耳中的活性起作用。最后,我们通过染色质免疫沉淀和共免疫沉淀表明,Sox5直接结合到SoxD/E位点,并且它可以与Sox8相互作用,进一步支持它们在躯干神经嵴中激活Sox10E1的组合作用。这些结果揭示了发育中的胚胎中Sox10表达的重要组织特异性输入。