{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,19]],"date-time":"2026-10-19T15:42:35Z","timestamp":1792424555576,"version":"4.5.0"},"reference-count":31,"publisher":"National Academy of Sciences","issue":"8","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2002,4,16]]},"abstract":"<jats:p>\n                    Retinitis pigmentosa (RP), a common group of human retinopathic diseases, is characterized by late-onset night blindness, loss of peripheral vision, and diminished or absent electroretinogram (ERG) responses. Mutations in the photoreceptor-specific gene\n                    <jats:italic>RP1<\/jats:italic>\n                    account for 5\u201310% of cases of autosomal dominant RP. We generated a mouse model of the RP1 form of RP by targeted disruption of the mouse ortholog (\n                    <jats:italic>Rp1<\/jats:italic>\n                    ) of human\n                    <jats:italic>RP1<\/jats:italic>\n                    . In\n                    <jats:italic>Rp1<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice, the number of rod photoreceptors decreased progressively over a period of 1 year, whereas that of cone photoreceptors did not change for at least 10 months. Light and electron microscopic analysis revealed that outer segments of\n                    <jats:italic>Rp1<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    rods and cones were morphologically abnormal and became progressively shorter in length. Before photoreceptor cell death, rhodopsin was mislocalized in inner segments and cell bodies of\n                    <jats:italic>Rp1<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    rods. Rod ERG amplitudes of\n                    <jats:italic>Rp1<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice were significantly smaller than those of\n                    <jats:italic>Rp1<\/jats:italic>\n                    <jats:sup>+\/+<\/jats:sup>\n                    mice over a period of 12 months, whereas those of\n                    <jats:italic>Rp1<\/jats:italic>\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice were intermediate. The decreases in cone ERG amplitudes were slower and less severe than those in rods. These findings demonstrate that Rp1 is required for normal morphogenesis of photoreceptor outer segments and also may play a role in rhodopsin transport to the outer segments. The phenotype of\n                    <jats:italic>Rp1<\/jats:italic>\n                    mutant mice resembles the human RP1 disease. Thus, these mice provide a useful model for studies of RP1 function, disease pathology, and therapeutic interventions.\n                  <\/jats:p>","DOI":"10.1073\/pnas.042122399","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:45:09Z","timestamp":1027680309000},"page":"5698-5703","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":106,"title":["Progressive photoreceptor degeneration, outer segment dysplasia, and rhodopsin mislocalization in mice with targeted disruption of the retinitis pigmentosa-1 (\n                    <i>Rp1<\/i>\n                    ) gene"],"prefix":"10.1073","volume":"99","author":[{"given":"Jiangang","family":"Gao","sequence":"first","affiliation":[{"name":"Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105; Department of Anatomy and Neurobiology, University of Tennessee, Memphis, TN 38163; Jules Stein Eye Institute, University of California School of Medicine, Los Angeles, CA 90095-7000; F. M. Kirby Center for Molecular Ophthalmology, Scheie Eye Institute, Philadelphia, PA 19104; and Human Genetics Center, School of Public Health, and Department of Ophthalmology and Visual Science, University of Texas..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kyeongmi","family":"Cheon","sequence":"additional","affiliation":[{"name":"Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105; Department of Anatomy and Neurobiology, University of Tennessee, Memphis, TN 38163; Jules Stein Eye Institute, University of California School of Medicine, Los Angeles, CA 90095-7000; F. M. Kirby Center for Molecular Ophthalmology, Scheie Eye Institute, Philadelphia, PA 19104; and Human Genetics Center, School of Public Health, and Department of Ophthalmology and Visual Science, University of Texas..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Steven","family":"Nusinowitz","sequence":"additional","affiliation":[{"name":"Department of Developmental Neurobiology, St. Jude Children's Research Hospital, Memphis, TN 38105; Department of Anatomy and Neurobiology, University of Tennessee, Memphis, TN 38163; Jules Stein Eye Institute, University of California School of Medicine, Los Angeles, CA 90095-7000; F. M. 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