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This eliminated the light-dependent phosphorylation of rhodopsin and caused the single-photon response to become larger and longer lasting than normal. These results demonstrate that RK is required for normal rhodopsin deactivation. When the photon responses of RK\u2212\/\u2212 rods did finally turn off, they did so abruptly and stochastically, revealing a first-order backup mechanism for rhodopsin deactivation. The rod outer segments of RK\u2212\/\u2212 mice raised in 12-hr cyclic illumination were 50% shorter than those of normal (RK+\/+) rods or rods from RK\u2212\/\u2212 mice raised in constant darkness. One day of constant light caused the rods in the RK\u2212\/\u2212 mouse retina to undergo apoptotic degeneration. Mice lacking RK provide a valuable model for the study of Oguchi disease, a human RK deficiency that causes congenital stationary night blindness.\n                  <\/jats:p>","DOI":"10.1073\/pnas.96.7.3718","type":"journal-article","created":{"date-parts":[[2002,7,26]],"date-time":"2002-07-26T10:42:40Z","timestamp":1027680160000},"page":"3718-3722","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":274,"title":["Abnormal photoresponses and light-induced apoptosis in rods lacking rhodopsin kinase"],"prefix":"10.1073","volume":"96","author":[{"given":"Ching-Kang","family":"Chen","sequence":"first","affiliation":[{"name":"Division of Biology, 147-75, California Institute of Technology, Pasadena, CA 91125; Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305; Howard Hughes Medical Institute and Department of Biochemistry, Box 357370, University of Washington, Seattle, WA 98195; and Department of Cell 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