The findings suggest that the non-image-forming pathway is functional long before the mainstream image-forming pathway during development.

Here, we show that (1) Prkcz plays an as yet unidentified role in melanopsin signaling, (2) the proteins of seven further light-regulated genes emerge as strong candidates in melanopsin signaling, and (3) transcriptional recalibration may provide a powerful new approach for dissecting unmapped signaling pathways.

The aims of this study were to address three related questions: (1) Do the photosensitive ganglion cells of the mouse convey light information to the suprachiasmatic nuclei (SCN) at P0? (2) Do the differentiating rods and cones contribute to light-evoked FOS induction within the murine SCN at P4? (3) How does light-evoked FOS induction within the SCN of melanopsin knockout (Opn4-/-) mice differ at P4 and P14? Our approaches took advantage of the published descriptions of murine ocular development, melanopsin knockout (Opn4-/-) mouse, and light-induced expression of FOS (the phosphoprotein product of immediate early gene c-fos) within the SCN as a marker of retinohypothalamic tract competence. Collectively, our results show that photosensitive melanopsin-dependent retinal ganglion cells provide light information to the murine SCN on the day of birth, and possibly beforehand, and that developing rods and cones fail to provide light information to the SCN during early postnatal life. On the basis of previous publications and data presented here, we suggest that at ages around P14 the rods and cones might be capable of fully compensating for the loss of melanopsin-photosensitive ganglion cells if exposure to light is of sufficiently long duration. These results are related to the broader context of recent findings and the potential role(s) of a neonatal photoreceptor.