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. Overall design: Comparative gene expression profiling analysis of RNA-seq data for biological replicates of E12.5 Vsx2<orJ/orj> retinas,  E12.5 Vsx2<orJ/orj>; Mitf<mi/+> retinas, and E12.5 Vsx2<orJ/+>; Mitf<+/+> retinas (control)