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Neuron. 2006 Jan 19;49(2):229-41.

Calnexin is essential for rhodopsin maturation, Ca2+ regulation, and photoreceptor cell survival.

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1
Department of Ophthalmology and Visual Sciences, Department of Genetics, University of Wisconsin, Madison, Wisconsin 53792, USA.

Abstract

In sensory neurons, successful maturation of signaling molecules and regulation of Ca2+ are essential for cell function and survival. Here, we demonstrate a multifunctional role for calnexin as both a molecular chaperone uniquely required for rhodopsin maturation and a regulator of Ca2+ that enters photoreceptor cells during light stimulation. Mutations in Drosophila calnexin lead to severe defects in rhodopsin (Rh1) expression, whereas other photoreceptor cell proteins are expressed normally. Mutations in calnexin also impair the ability of photoreceptor cells to control cytosolic Ca2+ levels following activation of the light-sensitive TRP channels. Finally, mutations in calnexin lead to retinal degeneration that is enhanced by light, suggesting that calnexin's function as a Ca2+ buffer is important for photoreceptor cell survival. Our results illustrate a critical role for calnexin in Rh1 maturation and Ca2+ regulation and provide genetic evidence that defects in calnexin lead to retinal degeneration.

PMID:
16423697
PMCID:
PMC3414428
DOI:
10.1016/j.neuron.2005.12.011
[Indexed for MEDLINE]
Free PMC Article

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