A framework to identify functional interactors that contribute to disrupted early retinal development in Vsx2 mutant mice III

These datasets contain the transcriptomes from E12.5 mouse retinal tissues from embryos carrying three different combinations of the Vsx2 ocular retardation J (orJ) allele and the Mitf mi (mi) allele: orJ-heterozygous, which serves as the control, orJ-homozygous, and orJ-homozygous; mi-heterozygous. The orJ allele is a recessive loss of function and the mi allele is semi-dominant. Mitf is direct target of repression by Vsx2 in the retina and is an established causal factor in the orJ ocular phenotype of microphthalmia. The goal of this analysis was to determine if blocking Mitf function in the orJ mutant would restore retinal gene expression to wild type levels. All libraries were prepared and sequenced together, facilitating direct comparisons of the gene expression profiles across the 3 genotypes.本数据集涵盖携带三种不同Vsx2眼迟缓J（Vsx2 ocular retardation J, orJ）等位基因与Mitf mi（Mitf mi, mi）等位基因组合的E12.5天小鼠视网膜组织的转录组（transcriptome）：其中以orJ杂合子作为对照，其余两种基因型分别为orJ纯合子，以及orJ纯合且mi杂合子。orJ等位基因为隐性功能丧失突变，mi等位基因为半显性突变。Mitf是视网膜中受Vsx2抑制的直接靶标，亦是orJ突变体小眼畸形表型的已证实致病因素。本分析的核心目标为明确：在orJ突变体中阻断Mitf功能是否可使视网膜基因表达水平恢复至野生型标准。所有文库均同步制备并测序，从而能够直接比对三种基因型间的基因表达谱。