{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T01:50:01Z","timestamp":1788313801570,"version":"build-2803163510"},"reference-count":68,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2019,12,21]],"date-time":"2019-12-21T00:00:00Z","timestamp":1576886400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["RO1 EY028035"],"award-info":[{"award-number":["RO1 EY028035"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R01 EY025536"],"award-info":[{"award-number":["R01 EY025536"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["R21 EY027707"],"award-info":[{"award-number":["R21 EY027707"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"name":"West Virginia Lions Club Foundation"},{"name":"International Lions Club Foundation"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,2,1]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Retinitis pigmentosa (RP) is a debilitating blinding disease affecting over 1.5 million people worldwide, but the mechanisms underlying this disease are not well understood. One of the common models used to study RP is the retinal degeneration-10 (rd10) mouse, which has a mutation in Phosphodiesterase-6b (Pde6b) that causes a phenotype mimicking the human disease. In rd10 mice, photoreceptor cell death occurs with exposure to normal light conditions, but as demonstrated in this study, rearing these mice in dark preserves their retinal function. We found that inactivating rhodopsin signaling protected photoreceptors from degeneration suggesting that the pathway activated by this G-protein-coupled receptor is causing light-induced photoreceptor cell death in rd10 mice. However, inhibition of transducin signaling did not prevent the loss of photoreceptors in rd10 mice reared under normal light conditions implying that the degeneration caused by rhodopsin signaling is not mediated through its canonical G-protein transducin. Inexplicably, loss of transducin in rd10 mice also led to photoreceptor cell death in darkness. Furthermore, we found that the rd10 mutation in Pde6b led to a reduction in the assembled PDE6\u03b1\u03b2\u03b32 complex, which was corroborated by our data showing mislocalization of the \u03b3 subunit. Based on our findings and previous studies, we propose a model where light activates a non-canonical pathway mediated by rhodopsin but independent of transducin that sensitizes cyclic nucleotide gated channels to cGMP and causes photoreceptor cell death. These results generate exciting possibilities for treatment of RP patients without affecting their vision or the canonical phototransduction cascade.<\/jats:p>","DOI":"10.1093\/hmg\/ddz299","type":"journal-article","created":{"date-parts":[[2019,12,6]],"date-time":"2019-12-06T12:44:23Z","timestamp":1575636263000},"page":"394-406","source":"Crossref","is-referenced-by-count":17,"title":["Rhodopsin signaling mediates light-induced photoreceptor cell death in rd10 mice through a transducin-independent mechanism"],"prefix":"10.1093","volume":"29","author":[{"given":"Jesse C","family":"Sundar","sequence":"first","affiliation":[{"name":"Departments of Biochemistry, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV 26505, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniella","family":"Munezero","sequence":"additional","affiliation":[{"name":"Departments of Ophthalmology and Visual Sciences, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV 26505, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Caitlyn","family":"Bryan-Haring","sequence":"additional","affiliation":[{"name":"Departments of Biochemistry, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV 26505, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thamaraiselvi","family":"Saravanan","sequence":"additional","affiliation":[{"name":"Departments of Ophthalmology and Visual Sciences, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV 26505, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angelica","family":"Jacques","sequence":"additional","affiliation":[{"name":"Departments of Ophthalmology and Visual Sciences, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV 26505, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Visvanathan","family":"Ramamurthy","sequence":"additional","affiliation":[{"name":"Departments of Biochemistry, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV 26505, USA"},{"name":"Departments of Ophthalmology and Visual Sciences, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV 26505, USA"},{"name":"Departments of Neuroscience, Robert C. Byrd Health Sciences Center, West Virginia University, Morgantown, WV 26505, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2019,12,21]]},"reference":[{"key":"2020021222131451500_ref1","first-page":"1","volume-title":"GeneReviews\u00ae [Internet]","author":"Fahim","year":"2017"},{"key":"2020021222131451500_ref2","doi-asserted-by":"crossref","first-page":"238","DOI":"10.2174\/138920211795860107","article-title":"Retinitis pigmentosa: genes and disease mechanisms","volume":"12","author":"Ferrari","year":"2011","journal-title":"Curr. 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