Rods, not ipRGCs, are the major retinal photoreceptor impacting development of dopaminergic signaling in the retina.

Skin cells from a patient with retinitis pigmentosa have been used to generate induced pluripotent stem cells, which could potentially form the basis of new treatments for this disease.

The integrated analysis of multi-omics and functional evidence both in vitro and in knock-in mouse models reveal novel gain-of-function pathogenic mechanisms of dominant CRX HD missense mutations.

Dominant mutations in Arl3, linked to inherited retinal dystrophy, disrupt the active Arl3-GTP ciliary gradient and cause a defect in rod photoreceptor nuclear migration that can be rescued by elevating ciliary Arl3 activity or reducing aberrant non-ciliary Arl3 activity.

NMNAT1, a ubiquitously expressed metabolic enzyme linked to inherited blinding disease, is crucial for the proper differentiation of photoreceptor cells and subsequent survival of multiple cell types in the retina.

Tools and resources to identify transcriptional regulators that create and maintain differences between photoreceptor subtypes.

Silencers and enhancers targeted by a common transcription factor in photoreceptors are distinguished by the number and diversity of binding transcription factor binding sites they contain.

Genome-wide analysis of DNA methylation and accessible chromatin shows that retinal rods and cones have distinct epigenomic features that reflect differences in their development and function.

R7 photoreceptors require the endosomal protein Lost and Found to form stable connections only when this protein is also present in neurons that are synaptic partners of R7.

Formation of a triangular lattice of photoreceptor clusters in the compound eye is driven by highly regulated cell flows in the eye epithelium, through a mechanochemical mechanism.