MYT1L loss leads to chromatin structures and transcriptome alterations in mouse hypothalamus [RNA-Seq]

MYT1L Syndrome mouse model displays obesity as observed in MYT1L patients. Utilizing this mouse model, ATAC-seq and RNA-seq on adult mouse hypothalamus reveals molecular alternations related to feeding behaviors, which might contribute to obesity phenotype. We have 3 biological replicates per genotype for ATAC-seq and 6(Het)/5(WT) replicates for RNA-seq on adult mouse hypothalamusMYT1L综合征小鼠模型可呈现出与MYT1L患者一致的肥胖表型。本研究依托该小鼠模型，对成年小鼠下丘脑开展ATAC-seq与RNA-seq测序分析，成功揭示了与摄食行为相关的分子改变，此类改变或为肥胖表型的潜在致病机制。本次实验中，针对成年小鼠下丘脑的ATAC-seq实验每个基因型均设置3次生物学重复；RNA-seq实验则分别为杂合子（Het）组设置6次生物学重复，野生型（WT）组设置5次生物学重复。