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Here we show that melanopsin coordinates retinohypothalamic tract development by regulating local translation in developing ipRGC axons. Loss of melanopsin selectively disrupted local translation in axons without affecting somatic translation. The affected transcripts encoded cytoskeletal regulators, adhesion molecules, and trafficking proteins, and activity-dependent changes in translation were restricted to the period before eye-opening. Consistent with impaired axonal growth and synaptogenesis,\n                  <jats:italic>Opn4<\/jats:italic>\n                  knockout mice showed reduced ipsilateral suprachiasmatic nucleus innervation and fewer retinohypothalamic synapses, while nanoscale synaptic molecular organization and microglial engulfment were unaffected. Reduced visual drive in\n                  <jats:italic>Opn4<\/jats:italic>\n                  knockouts further altered developmental gene expression programs across the retina, suprachiasmatic nucleus, and lateral geniculate nucleus, with region-specific differences in expression timing. These findings identify melanopsin as a regulator of local axonal translation during early circuit development, linking sensory phototransduction to translational control mechanisms that guide retinohypothalamic tract assembly and postsynaptic target maturation.\n                <\/jats:p>","DOI":"10.64898\/2026.04.21.716817","type":"posted-content","created":{"date-parts":[[2026,4,23]],"date-time":"2026-04-23T15:55:11Z","timestamp":1776959711000},"source":"Crossref","is-referenced-by-count":0,"title":["Melanopsin regulates axonal translation underlying retinohypothalamic circuit assembly"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9056-3242","authenticated-orcid":false,"given":"R.","family":"Rashmi","sequence":"first","affiliation":[{"name":"Department of Biology, University of Maryland, College Park, Maryland, USA 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