UTX Regulates Human Neural Differentiation and Dendritic Morphology by Resolving Bivalent Promoters

The loss of UTX impaired both the differentiation efficiency and morphogenesis of neurons. In further detection of the electrophysiological activity of neurons, the electrophysiological activity of neurons formed by UTX knockout cell lines was also significantly lower than that of the control group.
In order to further detect the differentially expressed genes and their histone modification changes in WT group and UTX-KO group, we collected DAY40 neurons for RNA-seq and ChIP-seq combined analysis, which confirmed that UTX can act as a demmethylation enzyme.
It affects the developmental process of the nervous system by regulating H3K27me3 on the dipromoter of related developmental genes.

UTX的缺失会同时损害神经元的分化效率与形态发生过程。后续针对神经元电生理活性的检测结果显示，由UTX敲除细胞系诱导形成的神经元，其电生理活性同样显著低于对照组。
为进一步检测野生型（WT）组与UTX敲除（UTX-KO）组中的差异表达基因及其组蛋白修饰变化，我们收集了培养至第40天的神经元样本，开展RNA测序（RNA-seq）与染色质免疫沉淀测序（ChIP-seq）联合分析，实验结果证实UTX可作为去甲基化酶。
该蛋白可通过调控相关发育基因启动子区域的H3K27me3修饰，进而影响神经系统的发育进程。