Transcriptional profiling of Setd5 mutant cortical neural progenitors

Setd5 inactivation in neural stem cells, zebrafish and mouse leads to a significant H3K36 hypo-methylation mostly detectable along the gene bodies. Consequently, this chromatin alteration perturbs RNA processing during elongation, compromising the transcriptional output. This gene dysregulation affects proliferative dynamics of NSCs and synaptic wiring in the neuronal derivatives, ultimately resulting in behavioral deficits in adult mice. 3 wt clones and 3 Setd5 het clones of NSC edited in Setd5 locus with CRISPR/Cas9在神经干细胞（neural stem cells, NSCs）、斑马鱼与小鼠体内，Setd5基因失活会诱发显著的H3K36低甲基化（H3K36 hypo-methylation），该表观修饰主要可在基因体区域被检测到。此类染色质改变会干扰转录延伸阶段的RNA加工进程，损害转录输出水平。该基因失调会影响NSCs的增殖动力学，并改变神经元子代细胞的突触连接模式，最终导致成年小鼠出现行为缺陷。本数据集包含3份通过CRISPR/Cas9对Setd5基因座进行编辑的NSCs野生型克隆，以及3份Setd5杂合克隆。