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Abnormal photoresponses and light-induced apoptosis in rods lacking rhodopsin kinase

Chen, Ching-Kang and Burns, Marie E. and Spencer, Maribeth and Niemi, Gregory A. and Chen, Jeannie and Hurley, James B. and Baylor, Denis A. and Simon, Melvin I. (1999) Abnormal photoresponses and light-induced apoptosis in rods lacking rhodopsin kinase. Proceedings of the National Academy of Sciences of the United States of America, 96 (7). pp. 3718-3722. ISSN 0027-8424. http://resolver.caltech.edu/CaltechAUTHORS:CHEpnas99b

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Abstract

Phosphorylation is thought to be an essential first step in the prompt deactivation of photoexcited rhodopsin. In vitro, the phosphorylation can be catalyzed either by rhodopsin kinase (RK) or by protein kinase C (PKC). To investigate the specific role of RK, we inactivated both alleles of the RK gene in mice. 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-/- 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-/- mice raised in 12-hr cyclic illumination were 50% shorter than those of normal (RK+/+) rods or rods from RK-/- mice raised in constant darkness. One day of constant light caused the rods in the RK-/- 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.


Item Type:Article
Additional Information:Copyright © 1999 by The National Academy of Sciences. Contributed by Melvin Simon, January 12, 1999. We thank members of the Caltech Transgenic Core Facility for their technical support. We also thank Wolfgang Baehr for the mouse retinal cDNA library. This work was supported by grants from the National Institute of Aging (M.I.S.), the National Eye Institute (D.A.B. and J.B.H.), the McKnight Foundation (D.A.B.), and the Ruth and Milton Steinbach fund (D.A.B.). Data deposition: The sequence reported in this paper has been deposited in the GenBank database (accession no. AF085240). C.-K.C. and M.E.B. contributed equally to this work. The publication costs of this article were defrayed in part by page charge payment. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. §1734 solely to indicate this fact.
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Funding AgencyGrant Number
National Institute of AgingUNSPECIFIED
National Eye InstituteUNSPECIFIED
McKnight FoundationUNSPECIFIED
Ruth and Milton Steinbach fundUNSPECIFIED
Record Number:CaltechAUTHORS:CHEpnas99b
Persistent URL:http://resolver.caltech.edu/CaltechAUTHORS:CHEpnas99b
Alternative URL:http://www.pnas.org/cgi/content/abstract/96/7/3718
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:810
Collection:CaltechAUTHORS
Deposited By: Archive Administrator
Deposited On:07 Oct 2005
Last Modified:26 Dec 2012 08:41

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