A framework to identify functional interactors that contribute to disrupted early retinal development in Vsx2 mutant mice I
These datasets contain the transcriptomes from E12.5 orJ-homozygous (orJ mutant) retinal tissues after organotypic culture of retina and lens for 24 hours in the presence or absence of the gamma-Secretase inhibitor Dibenzazipine (DBZ). A trait of the orJ mutant retina is the persistence of retinal progenitor cells (RPCs) during development despite greatly reduced proliferation and delayed neurogenesis. This led us to test whether gamma secretase activity was maintaining the RPC population in the orJ mutant retina, possibly through Notch signaling. The goal of this analysis was to determine if blocking gamma-Secretase activity would shift RPCs from a progenitor to a neurogenic state by comparing the retinal gene expression profiles of biological replicates from 300 nM DBZ-treated and vehicle-treated (0.1% DMSO) cultures. Overall design: Comparative gene expression profiling analysis of RNA-seq data for biological replicates of E12.5 Vsx2<orJ/orj> mutant retinas treated with the gamma secretase inhibitor Dibenzazepine (DBZ) compared to vehicle control (Dimethyl Sulfoxide).