MYT1L loss leads to chromatin structures and transcriptome alterations in mouse hypothalamus [RNA-Seq]. 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. Overall design: We have 3 biological replicates per genotype for ATAC-seq and 6(Het)/5(WT) replicates for RNA-seq on adult mouse hypothalamus

MYT1L综合征（MYT1L Syndrome）小鼠模型可呈现肥胖表型，该表型与MYT1L患者的临床表现一致。本研究依托该小鼠模型，对成年小鼠下丘脑组织开展ATAC-seq（转座酶可及性染色质测序）与RNA-seq（RNA测序）分析，成功揭示了与摄食行为相关的分子调控异常，此类异常或为肥胖表型的潜在致病机制。总体实验设计：针对两种基因型的成年小鼠下丘脑样本，我们为每种基因型的ATAC-seq设置了3个生物学重复；RNA-seq则包含6个杂合型（Het）样本与5个野生型（WT）样本的生物学重复。