Lillehei Heart Institute, University of Minnesota, Minneapolis, MN, 55455, USA.
Stem Cell Institute, University of Minnesota, Minneapolis, MN, 55455, USA.
Nat Commun. 2022 Jul 21;13(1):4221. doi: 10.1038/s41467-022-31848-6.
Sonic hedgehog (Shh) is essential for limb development, and the mechanisms that govern the propagation and maintenance of its expression has been well studied; however, the mechanisms that govern the initiation of Shh expression are incomplete. Here we report that ETV2 initiates Shh expression by changing the chromatin status of the developmental limb enhancer, ZRS. Etv2 expression precedes Shh in limb buds, and Etv2 inactivation prevents the opening of limb chromatin, including the ZRS, resulting in an absence of Shh expression. Etv2 overexpression in limb buds causes nucleosomal displacement at the ZRS, ectopic Shh expression, and polydactyly. Areas of nucleosome displacement coincide with ETS binding site clusters. ETV2 also functions as a transcriptional activator of ZRS and is antagonized by ETV4/5 repressors. Known human polydactyl mutations introduce novel ETV2 binding sites in the ZRS, suggesting that ETV2 dosage regulates ZRS activation. These studies identify ETV2 as a pioneer transcription factor (TF) regulating the onset of Shh expression, having both a chromatin regulatory role and a transcriptional activation role.
声波刺猬(Shh)对于肢体发育是必需的,其表达的传播和维持的机制已得到很好的研究;然而,调控 Shh 表达起始的机制尚不完全清楚。在这里,我们报告 ETV2 通过改变发育性肢体增强子 ZRS 的染色质状态来启动 Shh 表达。Etv2 在肢体芽中先于 Shh 表达,并且 Etv2 的失活阻止了肢体染色质的打开,包括 ZRS,导致 Shh 表达缺失。Etv2 在肢体芽中的过表达导致 ZRS 处核小体位移、异位 Shh 表达和多指。核小体位移的区域与 ETS 结合位点簇重合。ETV2 也是 ZRS 的转录激活因子,并且受到 ETV4/5 抑制剂的拮抗。已知的人类多指突变在 ZRS 中引入新的 ETV2 结合位点,这表明 ETV2 剂量调节 ZRS 的激活。这些研究确定 ETV2 为调节 Shh 表达起始的先驱转录因子(TF),具有染色质调节作用和转录激活作用。