Metabolic maturation during muscle stem cell differentiation is achieved by miR-1/133a-mediated inhibition of the Dlk-Dio3 mega gene cluster

Muscle-specific ablation of miR-1/133a expression leads to increased expression of miR-1/133a target genes at RNA and/or protein level. MEF2A is a direct target of miR-1/133a that is upregulated at the protein level and subsequently activates the expression of the Dlk1-Dio3 cluster in skeletal muscle of miR-1/133a deficient mice. miRNAs encoded in the Dlk1-Dio3 cluster directly repress the expression of multiple genes important for mitochondrial function. The study includes transcriptome analysis of tibialis anterior muscle after muscle-specific deletion of miR-1/133a as well as transcriptome analysis of tibialis anterior muscle after muscle-specific overexpression of Mef2A.对微小RNA-1/133a（miR-1/133a）实施肌肉特异性敲除，可导致其靶基因在RNA及/或蛋白水平的表达上调。肌细胞增强因子2A（MEF2A）是miR-1/133a的直接靶基因，其在蛋白水平表达上调后，可激活miR-1/133a缺陷小鼠骨骼肌中Dlk1-Dio3基因簇的表达。Dlk1-Dio3基因簇编码的微小RNA（miRNA），可直接抑制多种对线粒体功能至关重要的基因的表达。本数据集包含miR-1/133a肌肉特异性缺失后的胫骨前肌转录组分析数据，以及肌细胞增强因子2A（Mef2A）肌肉特异性过表达后的胫骨前肌转录组分析数据。