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Mechanisms of rhodopsin inactivation in vivo as revealed by a COOH-terminal truncation mutant

Chen, Jeannie and Makino, Clint L. and Peachey, Neal S. and Baylor, Denis A. and Simon, Melvin I. (1995) Mechanisms of rhodopsin inactivation in vivo as revealed by a COOH-terminal truncation mutant. Science, 267 (5196). pp. 374-377. ISSN 0036-8075. doi:10.1126/science.7824934. https://resolver.caltech.edu/CaltechAUTHORS:20150115-124616145

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Abstract

Although biochemical experiments suggest that rhodopsin and other receptors coupled to heterotrimeric guanosine triphosphate-binding proteins (G proteins) are inactivated by phosphorylation near the carboxyl (COOH)-terminus and the subsequent binding of a capping protein, little is known about the quenching process in vivo. Flash responses were recorded from rods of transgenic mice in which a fraction of the rhodopsin molecules lacked the COOH-terminal phosphorylation sites. In the single photon regime, abnormally prolonged responses, attributed to activation of individual truncated rhodopsins, occurred interspersed with normal responses. The occurrence of the prolonged responses suggests that phosphorylation is required for normal shutoff. Comparison of normal and prolonged single photon responses indicated that rhodopsin begins to be quenched before the peak of the electrical response and that quenching limits the response amplitude.


Item Type:Article
Related URLs:
URLURL TypeDescription
http://dx.doi.org/10.1126/science.7824934DOIArticle
http://www.sciencemag.org/content/267/5196/374PublisherArticle
http://www.jstor.org/stable/2886245JSTORArticle
Additional Information:© 1995 American Association for the Advancement of Science. 21 June 1994; Accepted 10 November 1994. We thank T. Nakayama for making the transgene construct and B. Kobilka for his critique of an earlier version of the manuscript. The care and treatment of animals used in this study conformed to protocols approved by the respective institutions. Supported by the Ruth and Milton Steinbach Fund, the Department of Veteran's Affairs, the National Eye Institute (grants EY0570 and F32 EY06405), and the National Institute of Aging (NIH grant AG 12288).
Funders:
Funding AgencyGrant Number
Ruth and Milton Steinbach fundUNSPECIFIED
Department of Veterans AffairsUNSPECIFIED
National Eye InstituteEY0570
National Eye InstituteF32 EY06405
National Institute of AgingUNSPECIFIED
NIHAG12288
Issue or Number:5196
DOI:10.1126/science.7824934
Record Number:CaltechAUTHORS:20150115-124616145
Persistent URL:https://resolver.caltech.edu/CaltechAUTHORS:20150115-124616145
Official Citation:Chen, J., Makino, C., Peachey, N., Baylor, D., & Simon, M. (1995). Mechanisms of rhodopsin inactivation in vivo as revealed by a COOH-terminal truncation mutant. Science, 267(5196), 374-377. doi: 10.1126/science.7824934
Usage Policy:No commercial reproduction, distribution, display or performance rights in this work are provided.
ID Code:53787
Collection:CaltechAUTHORS
Deposited By: Joanne McCole
Deposited On:16 Jan 2015 00:59
Last Modified:10 Nov 2021 20:07

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