Depletion of miR-96 delays, but does not arrest, photoreceptor development in mice

Abundant retinal miR-183C (composed of miR-182, miR-183 and miR-96) has attracted the attention of researchers in the past decade. Our group has a great interest in uncovering the individual role of retinal miRNAs in this cluster. Among these sister miRNAs, miR-96 is expressed at the lowest and almost undetectable levels in cones, and mutations in the seed sequences only cause hearing defects but not serious vision impairment in patients. All this important information led us to study miR-182 and miR-183. However, we feel that we have to fully evaluate the remaining miRNA, miR-96, in the retina before we move forward to discuss the other possibilities. To identify which genes and pathways in the retina were affected by the depletion of miR-96, a whole-retinal RNA-seq analysis was conducted at P120. Hopefully, this data will be useful for the potential readers and the colleagues to compare the expression differences between miR-96, miR-183C and even the other single miRNA in this cluster.