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Circadian clock control of connexin36 phosphorylation in retinal photoreceptors of the CBA/CaJ mouse strain

Published online by Cambridge University Press:  20 May 2015

ZHIJING ZHANG
Affiliation:
Department of Ophthalmology and Visual Science, University of Texas Health Science Center at Houston, Medical School, Houston, Texas
HONGYAN LI
Affiliation:
Department of Neurobiology and Anatomy, University of Texas Health Science Center at Houston, Medical School, Houston, Texas
XIAOQIN LIU
Affiliation:
Department of Neurobiology and Anatomy, University of Texas Health Science Center at Houston, Medical School, Houston, Texas
JOHN O'BRIEN
Affiliation:
Department of Ophthalmology and Visual Science, University of Texas Health Science Center at Houston, Medical School, Houston, Texas Graduate School of Biomedical Sciences, University of Texas Health Science Center at Houston, Houston, Texas Program in Neuroscience, Graduate School of Biomedical Sciences, The University of Texas Health Science Center at Houston, Houston, Texas Neuroscience Research Center, The University of Texas Health Science Center at Houston, Houston, Texas
CHRISTOPHE P. RIBELAYGA*
Affiliation:
Department of Ophthalmology and Visual Science, University of Texas Health Science Center at Houston, Medical School, Houston, Texas Graduate School of Biomedical Sciences, University of Texas Health Science Center at Houston, Houston, Texas Program in Neuroscience, Graduate School of Biomedical Sciences, The University of Texas Health Science Center at Houston, Houston, Texas Neuroscience Research Center, The University of Texas Health Science Center at Houston, Houston, Texas
*
*Address correspondence to: Christophe P. Ribelayga, Ruiz Department of Ophthalmology and Visual Science, The University of Texas Medical School, 6431 Fannin St., MSB 7.024, Houston, TX 77030. E-mail: Christophe.p.ribelayga@uth.tmc.edu

Abstract

The gap-junction-forming protein connexin36 (Cx36) represents the anatomical substrate of photoreceptor electrical coupling in mammals. The strength of coupling is directly correlated to the phosphorylation of Cx36 at two regulatory sites: Ser110 and Ser293. Our previous work demonstrated that the extent of biotinylated tracer coupling between photoreceptor cells, which provides an index of the extent of electrical coupling, depends on the mouse strain. In the C57Bl/6J strain, light or dopamine reduces tracer coupling and Cx36 phosphorylation in photoreceptors. Conversely, darkness or a dopaminergic antagonist increases tracer coupling and Cx36 phosphorylation, regardless of the daytime. In the CBA/CaJ strain, photoreceptor tracer coupling is not only regulated by light and dopamine, but also by a circadian clock, a type of oscillator with a period close to 24 h and intrinsic to the retina, so that under prolonged dark-adapted conditions tracer coupling is broader at night compared to daytime. In the current study, we examined whether the modulation of photoreceptor coupling by a circadian clock in the CBA/CaJ mouse photoreceptors reflected a change in Cx36 protein expression and/or phosphorylation. We found no significant change in Cx36 expression or in the number of Cx36 gap junction among the conditions examined. However, we found that Cx36 phosphorylation is higher under dark-adapted conditions at night than in the daytime, and is the lowest under prolonged illumination at any time of the day/night cycle. Our observations are consistent with the view that the circadian clock regulation of photoreceptor electrical coupling is mouse strain-dependent and highlights the critical position of Cx36 phosphorylation in the control of photoreceptor coupling.

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Type
Brief Communication
Copyright
Copyright © Cambridge University Press 2015 

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